Major interaction on record — check this product against your medications before combining. Based on 16 of 42 ingredients. Check your meds →
Dietary supplement

Chandraprabha Vati Tablet Ingredients & Drug Interactions

by Vedic Supplements

Chandraprabha Vati Tablet label
See full label image
Tablet Or Pill Category: Other Combinations
Most serious interaction: Major
Clinical methodology reviewed by · Updated Sep 30, 2026 · Label data from the NIH DSLD
What is this page for?

First and foremost: checking Chandraprabha Vati Tablet against your medications. The heart of this page is the interaction checker and the full interaction report — how this product’s ingredients may interact with prescription and over-the-counter medicines you may be taking.

Around that, we add a pharmacist’s high-level view of the product as a whole — what’s inside, the evidence for its stated use, how transparent the label is, and what safety data exists — so you can see the full picture in one place. It’s educational information from our licensed clinical databases and the clinical staff at HelloPharmacist — not medical advice — and we don’t sell or endorse products. Our editorial policy

The interaction bottom line Most serious interaction: Major

Chandraprabha Vati Tablet is a dietary supplement by Vedic Supplements with 42 active ingredients. Its ingredients are commonly taken for preventing or treating magnesium deficiency, constipation, muscle cramps.Based on those ingredients, 1,619 medications have a known interaction with it, the most serious rated major. The ingredients most likely to interact are Daru Haldi, Turmeric, Chitraka. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.

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Check Your Meds Against Chandraprabha Vati Tablet by Vedic Supplements

Ask about any prescription or over-the-counter medication and we check it for interactions with Chandraprabha Vati Tablet by Vedic Supplements — and tell you which ingredient is responsible.

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HelloPharmacist Scorecard of Chandraprabha Vati Tablet by Vedic Supplements

Our pharmacy team’s full take, with four database checks built into the cards below — a summary of what is known, not a grade of the product itself.

From our pharmacy team — supplement deep dive

Generated from HelloPharmacist’s pharmacist-curated databases and editorial rules · Last generated Jul 11, 2026

What’s inside

Low disclosure
Ingredient Transparency · database check
Low

Most active ingredients don't disclose an individual amount — you can't tell how much of each you're getting.

Why this rating?
  • The label discloses an exact amount for 0 of its 42 active ingredients.
  • “Ingredients” is listed as a grouped ingredient — the label doesn't break down how much of each component you get.

Chandraprabha Vati contains 42 ingredients total. The active ones are traditional Ayurvedic herbs and minerals: Magnesium stearate (a mineral), Sodium starch glycolate (a sodium salt), Pippali and Pippali Mool (Indian long pepper), Sunthi (ginger), Kalmegh (andrographis), Giloy (Tinospora cordifolia), Turmeric, Daru Haldi (tree turmeric), Chitraka (Ceylon leadwort), and several others including Haritaki, Nagarmotha, and traditional spices like Dalchini (cinnamon) and Choti Elaichi (cardamom).

The product also contains inactive ingredients (fillers and binders) to hold the tablet together.

Does it work?

Not established
Evidence for Intended Use · database check
By FDA rules, dietary supplements can’t claim to treat, cure, or prevent disease — so labels speak in careful marketing language. We discern each product’s intended use from its name, label claims, and label statements, then grade the clinical evidence for that use. How these ratings are computed
Not established

The graded evidence we hold for these ingredients covers different conditions than the ones this product is marketed for, so there's no established rating for its stated use.

Why this rating?
  • The label markets this product for: Healthy urinary tract support.
  • We looked for evidence on: Urinary tract infection, Cystitis, Urinary health.
  • The closest evidence on file: Ceylon Cinnamon is rated "Insufficient Reliable Evidence To Rate" for Intestinal parasite infection (Natural Medicines).
  • Also on file: Turmeric is rated "Insufficient Reliable Evidence To Rate" for Respiratory tract infections.
  • Also on file: Ginger is rated "Insufficient Reliable Evidence To Rate" for Upper respiratory tract infection (URTI).

The evidence for Chandraprabha Vati as a whole product is not established in our data. However, some of its individual ingredients have effectiveness ratings.

Magnesium is effective for dyspepsia (indigestion) and constipation. Ginger is possibly effective for pregnancy-related nausea and vomiting, menstrual cramps, and osteoarthritis, though it was found possibly ineffective for exercise-induced muscle soreness.

Andrographis is possibly effective for ulcerative colitis, sore throat, and osteoarthritis. Tinospora cordifolia is possibly effective for type 2 diabetes.

Turmeric is possibly effective for depression, high cholesterol, and allergic rhinitis (hay fever). For most other claimed uses, evidence is insufficient or hasn't been established in the data we hold.

The evidence, ingredient by ingredient Magnesium Sodium Indian Long Pepper Ginger Andrographis Tinospora Cordifolia Turmeric Aconite

How safe is it?

Well-documented data
Safety Information · database check
Well characterized

Adverse-effect, pregnancy, and general safety data are on file for most of these ingredients.

Why this rating?
  • We hold adverse-effect (side-effect) data for 13 of the 16 matched ingredients.
  • Pregnancy & breastfeeding safety ratings cover 16 of 16.
  • General safety write-ups exist for 16 of 16.
  • Remember: this measures how much safety information exists. Thin data is not the same as being safe.

Magnesium is generally well tolerated at typical doses; common side effects include diarrhea, nausea, and gastrointestinal discomfort. Sodium should be limited—too much is linked to high blood pressure and heart strain; the product contains sodium starch glycolate, so it contributes dietary sodium.

Ginger is generally well tolerated, though higher doses increase side effects; it may cause heartburn, diarrhea, or mouth irritation. Andrographis is usually well tolerated short-term but quality and long-term safety aren't well established; rash and allergic reactions (including rare anaphylaxis) have been reported.

Tinospora cordifolia has raised concerns about liver injury in case reports; 49 patients developed hepatitis or acute liver failure after 6–12 weeks of use, with two requiring transplant and four dying. Turmeric is generally well tolerated as a food but concentrated supplements can cause constipation, nausea, and diarrhea; liver injury has been reported with supplement use for at least 2 weeks.

Daru Haldi (tree turmeric) has limited human safety data. Several ingredients lack adequate safety information for pregnancy and breastfeeding.

Side effects, ingredient by ingredient Magnesium Sodium Indian Long Pepper Ginger Andrographis Tinospora Cordifolia Turmeric Aconite

Meds to double-check

Major interaction found
Known Interaction Concern · database check
Major identified

At least one ingredient has a documented Major-severity interaction. Check your medications for a personalized result.

Why this rating?
  • 15 of the 16 matched ingredients can interact with medications — Ceylon Cinnamon, Indian Long Pepper, Aconite, Turmeric, Indian Gooseberry, among others.
  • The most serious interaction on file is rated Major.
  • Some involve high-stakes drug classes: anticoagulant / antiplatelet drugs; immunosuppressants / transplant drugs; cancer treatments; diabetes medications; heart-rhythm medications; lithium; Parkinson's medications.
  • For scale: 1,620 individual medications appear in the full list. A big number alone doesn't make a product dangerous — what matters is whether YOUR medication is on it, so run yours through the interaction checker on this page.

Before taking Chandraprabha Vati, check if you take tacrolimus or cyclosporine (Major interactions with Daru Haldi). Also flag: levodopa/carbidopa for Parkinson's disease, skeletal muscle relaxants, blood pressure medications, diuretics, antidiabetic drugs, blood thinners (anticoagulants), heart drugs (calcium channel blockers, nifedipine, losartan), quinolone antibiotics, bisphosphonates, immunosuppressants, theophylline, pentobarbital, other cancer drugs, and hormone therapy.

These all carry Moderate interactions. Use our medication checker for your specific drugs.

Check your own medication Run your meds through the checker above

The bottom line

Scorecard at a glanceFormula with limited ingredient disclosure with no established evidence rating for its marketed use. Major medication interactions have been identified, and safety information is well characterized.

This is a traditional Ayurvedic formula with multiple active ingredients, each carrying documented medication interactions—especially serious ones with immunosuppressants and blood pressure drugs. If you take any prescription medications (particularly tacrolimus, cyclosporine, levodopa, blood thinners, or diabetes drugs), check your exact medications with our tool before starting.

The product also raises concerns about liver safety and contains sodium; talk to your pharmacist or doctor about whether it's appropriate for you.

Educational only — not medical advice; always confirm with your pharmacist. Our editorial policy · How we use AI

Assessment coverage: 17 of 42 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated Aug 22, 2025.

This Scorecard evaluates available label information, ingredient evidence, and known medication-safety considerations. It does not independently verify product identity, purity, potency, contamination, or manufacturing quality. How these ratings are computed

At a glance

General information

Key facts about Chandraprabha Vati Tablet, straight from the product label.

Brand Vedic Supplements
Barcode (UPC) 850049510578
Net contents 120 Tablet(s)
Market status On market
Date entered into DSLD Aug 22, 2025
DSLD ID 336176
Product type Other Combinations
Supplement form Tablet Or Pill
Dietary claims / uses All Other, Structure/Function
Intended target group(s) Vegetarian, Adult (18 - 50 Years), Gluten Free
From the label
Everything in this section is reproduced from the manufacturer’s own product label — it’s the label speaking, not HelloPharmacist. We show it so you can see exactly what the maker states; we don’t verify or endorse those statements.

Supplement Facts

The label details for Chandraprabha Vati Tablet by Vedic Supplements, sourced from the NIH Dietary Supplement Label Database.

Supplement Facts

Daily Value (DV) Target Group(s):
Adults and children 4 or more years of age
Minimum serving Sizes:
1 Tab(s)
Maximum serving Sizes:
1 Tab(s)
Servings per container
120
UPC/BARCODE
850049510578
IngredientAmount% DV
Magnesium Stearate0 NP--
Sodium Starch Glycolate0 NP--
Ingredients0 NP--
Maize Starch0 NP--
Haritaki0 NP--
Talcum0 NP--
Pippali0 NP--
Sunthi0 NP--
Shati0 NP--
Nagarmotha0 NP--
Kalmegh0 NP--
Giloy0 NP--
Devadaru0 NP--
Turmeric0 NP--
Ativisha0 NP--
Daru Haldi0 NP--
Pippali Mool0 NP--
Chitraka0 NP--
Nisoth0 NP--
Danti0 NP--
Tej Patra0 NP--
Dalchini0 NP--
Choti Elaichi0 NP--
Vanshlochan0 NP--
Dhaniya0 NP--
Harar0 NP--
Baheda0 NP--
Amla0 NP--
Chavya0 NP--
Vidanga0 NP--
Gaj Pippali0 NP--
Swarna Makshik Bhasma0 NP--
Kali Mirch0 NP--
Yava Kshara0 NP--
Sarji Kshara0 NP--
Saindhava lavana0 NP--
Kala Namak0 NP--
Vida Lavana0 NP--
Lauha Bhasma0 NP--
Sita0 NP--
Shilajit Extract, Dry0 NP--
Shuddha Guggulu0 NP--
Aerosil0 NP--

Tap any ingredient to jump to its full detail below.

Label statements
These statements are the manufacturer’s wording, reproduced from the product label — the label is saying it, not HelloPharmacist. We don’t verify or endorse them.
General Statements

For Comments/Feedback: [email protected] 1-612-88-VEDIC Also try our highest-quality Herbal Juices, Powders, Tablets and Raw Herbs Scan OR Code and Explore our product Range

Formulation

Ayurveda + Modern Research = Synergistic Blend Product of India Ancient Ayurveda Made with Research

100% Veg

Healthy Urinary Tract Support

Premium Quality Traditional Ayurvedic Preparations Sustainable Farming Practices

BPA Free No Preservatives Gluten Free

Seals/Symbols

100% Ayurvedic Product

FDA Statement of Identity

Dietary Supplement

Brand IP Statement(s)

Vedic Supplements Your health matters

Is this label outdated? Report a formula or label change and our pharmacy team will review it.

See for yourself

Chandraprabha Vati Tablet by Vedic Supplements label

The label scan from the NIH Dietary Supplement Label Database. Tap to enlarge.

Chandraprabha Vati Tablet label

Label images are published by the NIH Dietary Supplement Label Database for the version of this product on file. Always read your actual product label.

View the full label (PDF)
What’s inside

The Ingredients in Chandraprabha Vati Tablet by Vedic Supplements

These are the 42 active ingredients this product is made of. Select any to open its full monograph.

Serving size1 Tab(s) Dosage formTablet Or Pill Servings per container120 Amounts shown are per serving.

Most supplement products combine several ingredients, and a medication can interact with the product through any one of them. Each ingredient below shows whether it has known drug interactions.

Ingredients

0 NP per serving
Interaction report

Chandraprabha Vati Tablet by Vedic Supplements Drug Interactions

Want to check YOUR meds against Chandraprabha Vati Tablet?

Ask about interactions with your drugs in plain English — “Can I take it with lisinopril?” — and we find you the answer in seconds, ingredient by ingredient.

 Go to the checker
1,619Drugs
8 Major 1,608 Moderate 3 Minor

Ingredients driving the most interactions

Daru Haldi 1,160
Turmeric 1,133
Chitraka 1,097
Kali Mirch 1,019
Sunthi 1,007

Individual Drug Interactions

The ingredients in Chandraprabha Vati Tablet interact with 1,619 drugs. Click any drug to see the details.

15 of the 42 ingredients in Chandraprabha Vati Tablet interact with drugs. Each result below shows which ingredient is responsible. Daru Haldi Turmeric Chitraka Kali Mirch Sunthi Baheda Pippali Giloy Kalmegh Magnesium Stearate Ativisha Dalchini Amla Sodium Starch Glycolate Shilajit Extract, Dry

Each ingredient & the kinds of drugs it affects

For each ingredient in Chandraprabha Vati Tablet with known interactions, here are the types of medications they can affect. Open any type for the detail — or search your exact drug in the checker above.

Daru Haldi12 drug types · 1,160 drugs

Cyclosporine (Neoral, Sandimmune)

Berberine, a constituent of tree turmeric, can reduce metabolism of cyclosporine and increase serum levels.
Some clinical evidence suggests that berberine inhibits cytochrome P450 3A4 (CYP3A4), which metabolizes cyclosporine.

Likelihood Likely Evidence A
Tacrolimus (Prograf)

Berberine, a constituent of tree turmeric, can inhibit metabolism of tacrolimus and increase plasma levels.
Some clinical evidence suggests that berberine inhibits cytochrome P450 3A4 (CYP3A4), which metabolizes tacrolimus. In a 16-year-old patient with idiopathic nephrotic syndrome who was being treated with prednisone 40 mg/m2 and tacrolimus 6.5 mg twice daily, concomitant use of berberine, a constituent of tree turmeric, 200 mg three times daily increased plasma levels of tacrolimus from 8 to 22 ng/mL and increased serum creatinine levels from 0.7 to 1.2 mg/dL. Following a reduction of tacrolimus dosing to 3 mg daily, the blood concentration of tacrolimus decreased to 12 ng/mL and the serum concentration of creatinine decreased to 0.9 mg/dL.

Likelihood Likely Evidence D
Anticoagulant/Antiplatelet Drugs

Theoretically, tree turmeric might have additive effects when used with anticoagulant and antiplatelet drugs and increase the risk of bleeding.
In vitro and animal research suggest that berberine, a constituent of tree turmeric, can inhibit platelet aggregation.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, tree turmeric, taken alone or in combination with milk thistle, might increase the risk of hypoglycemia in patients taking antidiabetes drugs.
Clinical research shows that taking a product containing tree turmeric and milk thistle extracts can lower blood glucose levels, glycated hemoglobin (HbA1c), and insulin resistance in patients with type 2 diabetes, including those on antidiabetic agents. Additionally, clinical research suggests that berberine, a constituent of tree turmeric, can lower blood glucose levels.

Likelihood Probable Evidence A
Antihypertensive Drugs

Theoretically, taking tree turmeric along with antihypertensive drugs might have additive effects and increase the risk of hypotension.
Animal research suggests that berberine, a constituent of tree turmeric, can have hypotensive effects. Also, a meta-analysis of clinical research suggests that taking berberine in combination with amlodipine (Norvasc) can lower systolic and diastolic blood pressure when compared with taking amlodipine alone.

Likelihood Possible Evidence D
Cns Depressants

Theoretically, use of tree turmeric along with CNS depressants might increase the risk of additive therapeutic and adverse effects.
Animal research suggests that berberine, a constituent of tree turmeric, can have sedative effects.

Likelihood Possible Evidence D
Cytochrome P450 2C9 (Cyp2C9) Substrates

Theoretically, tree turmeric might increase the levels and clinical effects of drugs metabolized by CYP2C9.
Preliminary clinical evidence suggests that berberine, a constituent of tree turmeric, can inhibit CYP2C9.

Likelihood Possible Evidence B
Cytochrome P450 2D6 (Cyp2D6) Substrates

Theoretically, tree turmeric might increase the levels and clinical effects of drugs metabolized by CYP2D6.
In vitro research and preliminary clinical evidence suggest that berberine, a constituent of tree turmeric, can inhibit CYP2D6.

Likelihood Possible Evidence B
Cytochrome P450 3A4 (Cyp3A4) Substrates

Theoretically, tree turmeric might increase the levels and clinical effects of drugs that are substrates of CYP3A4.
In vitro research and preliminary clinical evidence suggest that berberine, a constituent of tree turmeric, moderately inhibits CYP3A4.

Likelihood Probable Evidence A
Dextromethorphan (Robitussin Dm, Others)

Theoretically, tree turmeric might increase levels of dextromethorphan and potentially increase the risk of adverse effects including drowsiness, confusion, and irritability.
Preliminary clinical research suggests that berberine, a constituent of tree turmeric, can inhibit cytochrome P450 2D6 (CYP2D6) activity and reduce the metabolism of dextromethorphan.

Likelihood Possible Evidence B
Midazolam (Versed)

Theoretically, tree turmeric might increase levels of midazolam and potentially increase the risk of adverse effects including sedation and respiratory depression.
Preliminary clinical evidence suggests that berberine, a constituent of tree turmeric, can inhibit cytochrome P450 3A4 (CYP3A4) activity and reduce metabolism of midazolam.

Likelihood Possible Evidence B
Pentobarbital (Nembutal)

Theoretically, tree turmeric might increase the sedative effects of pentobarbital.
Animal research suggests that berberine, a constituent of tree turmeric, can prolong pentobarbital-induced sleeping time.

Likelihood Possible Evidence D
Daru Haldi full monograph & interactions

Turmeric24 drug types · 1,133 drugs

Alkylating Agents

Turmeric has antioxidant effects. Theoretically, this may reduce the activity of chemotherapy drugs that generate free radicals. However, research is conflicting.
In vitro research suggests that curcumin, a constituent of turmeric, inhibits mechlorethamine-induced apoptosis of breast cancer cells by up to 70%. Also, animal research shows that curcumin inhibits cyclophosphamide-induced tumor regression. However, some in vitro research shows that curcumin does not affect the apoptosis capacity of etoposide. Also, other laboratory research suggests that curcumin might augment the cytotoxic effects of alkylating agents. Reasons for the discrepancies may relate to the dose of curcumin and the specific chemotherapeutic agent. Lower doses of curcumin might have antioxidant effects while higher doses might have pro-oxidant effects. More evidence is needed to determine what effect, if any, turmeric might have on alkylating agents.

Likelihood Possible Evidence D
Amlodipine (Norvasc)

Taking turmeric with amlodipine may increase levels of amlodipine.
Animal research shows that giving amlodipine 1 mg/kg as a single dose following the use of turmeric extract 200 mg/kg daily for 2 weeks increases the maximum concentration and area under the curve by 53% and 56%, respectively, when compared with amlodipine alone. Additional animal research shows that taking amlodipine 1 mg/kg with a curcumin 2 mg/kg pretreatment for 10 days increases the maximum concentration and area under the curve by about 2-fold when compared with amlodipine alone.

Likelihood Possible Evidence D
Anticoagulant/Antiplatelet Drugs

Turmeric may have antiplatelet effects and may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs. However, research is conflicting.
Curcumin, a constituent of turmeric, has demonstrated antiplatelet effects in vitro. Furthermore, two case reports have found that taking turmeric along with warfarin or fluindione was associated with an increased international normalized ratio (INR). However, one clinical study in healthy volunteers shows that taking curcumin 500 mg daily for 3 weeks, alone or with aspirin 100 mg, does not increase antiplatelet effects or bleeding risk. It is possible that the dose of turmeric used in this study was too low to produce a notable effect.

Likelihood Possible Evidence B
Antidiabetes Drugs

Theoretically, taking turmeric with antidiabetes drugs might increase the risk of hypoglycemia.
Animal research and case reports suggest that curcumin, a turmeric constituent, can reduce blood glucose levels in patients with diabetes. Furthermore, clinical research in adults with type 2 diabetes shows that taking curcumin 475 mg daily for 10 days prior to taking glyburide 5 mg decreased postprandial glucose levels for up to 24 hours when compared with glyburide alone, despite the lack of a significant pharmacokinetic interaction. Other clinical studies in patients with diabetes show that taking curcumin daily can reduce blood glucose levels when compared with placebo.

Likelihood Possible Evidence B
Antitumor Antibiotics

Turmeric has antioxidant effects. Theoretically, this may reduce the activity of chemotherapy drugs that generate free radicals. However, research is conflicting.
In vitro and animal research shows that curcumin, a constituent of turmeric, inhibits doxorubicin-induced apoptosis of breast cancer cells by up to 65%. However, curcumin does not seem to affect the apoptosis capacity of daunorubicin. In fact, some research shows that curcumin might augment the cytotoxic effects of antitumor antibiotics, increasing their effectiveness. Reasons for the discrepancies may relate to the dose of curcumin and the chemotherapeutic agent. Lower doses of curcumin might have antioxidant effects while higher doses might have pro-oxidant effects. More evidence is needed to determine what effects, if any, antioxidants such as turmeric have on antitumor antibiotics.

Likelihood Possible Evidence D
Cytochrome P450 3A4 (Cyp3A4) Substrates

Turmeric might increase or decrease levels of drugs metabolized by CYP3A4.
In vitro and animal research show that turmeric and its constituents curcumin and curcuminoids inhibit CYP3A4. Also, 8 case reports from the World Health Organization (WHO) adverse drug reaction database describe increased toxicity in patients taking turmeric and cancer medications that are CYP3A4 substrates, including everolimus, ruxolitinib, ibrutinib, and palbociclib, and bortezomib. In another case report, a transplant patient presented with acute nephrotoxicity and elevated tacrolimus levels after consuming turmeric powder at a dose of 15 or more spoonfuls daily for ten days prior. It was thought that turmeric increased levels of tacrolimus due to CYP3A4 inhibition.
Conversely, other in vitro research suggests that turmeric induces CYP3A4 activity, leading to reduced levels of CYP3A4 substrates. An animal model suggests that induction of CYP3A4 occurs after daily curcumin use for 1 week. However, the induction of CYP3A4 by turmeric has not been reported in humans.

Likelihood Possible Evidence D
Hepatotoxic Drugs

Theoretically, turmeric might increase the risk of liver damage when taken with hepatotoxic drugs.
There is concern that turmeric might cause hepatotoxicity, especially when highly bioavailable formulations are used in high doses.

Likelihood Possible Evidence D
Methotrexate (Trexall, Others)

Theoretically, turmeric might have additive effects when used with hepatotoxic drugs such as methotrexate.
In one case report, a 39-year-old female taking methotrexate, turmeric, and linseed oil developed hepatotoxicity.

Likelihood Possible Evidence D
Organic Anion-Transporting Polypeptide Substrates (Oatp)

Theoretically, turmeric might increase blood levels of OATP4C1 substrates.
In vitro research shows that the turmeric constituent curcumin competitively inhibits OATP4C1 transport. This transporter is expressed in the kidney and facilitates the renal excretion of certain drugs. Theoretically, taking turmeric might decrease renal excretion of OATP substrates.

Likelihood Possible Evidence D
Sulfasalazine (Azulfidine)

Turmeric might increase the effects and adverse effects of sulfasalazine.
Clinical research shows that taking the turmeric constituent, curcumin, can increase blood levels of sulfasalazine by 3.2-fold.

Likelihood Probable Evidence B
Tacrolimus (Prograf)

Turmeric might increase the effects and adverse effects of tacrolimus.
In one case report, a transplant patient presented with acute nephrotoxicity and elevated tacrolimus levels of 29 ng/mL. The patient previously had tacrolimus levels within the therapeutic range at 9.7 ng/mL. Ten days prior to presenting at the emergency room the patient started consumption of turmeric powder at a dose of 15 or more spoonfuls daily. It was thought that turmeric increased levels of tacrolimus due to cytochrome P450 3A4 (CYP3A4) inhibition. In vitro and animal research show that turmeric and its constituent curcumin inhibit CYP3A4.

Likelihood Possible Evidence D
Talinolol

Turmeric may reduce the absorption of talinolol in some situations.
Clinical research shows that taking curcumin for 6 days decreases the bioavailability of talinolol when taken together on the seventh day. The clinical significance of this effect is unclear.

Likelihood Probable Evidence B
Tamoxifen (Nolvadex)

Theoretically, turmeric might reduce the levels and clinical effects of tamoxifen.
In a small clinical trial in patients with breast cancer taking tamoxifen 20-30 mg daily, adding curcumin 1200 mg plus piperine 10 mg three times daily reduces the 24-hour area under the curve of tamoxifen and the active metabolite endoxifen by 12.8% and 12.4%, respectively, as well as the maximum concentrations of tamoxifen, when compared with tamoxifen alone. However, in the absence of piperine, the area under the curve for endoxifen and the maximum concentration of tamoxifen were not significantly reduced. Effects were most pronounced in patients who were extensive cytochrome P450 (CYP) 2D6 metabolizers.

Likelihood Possible Evidence B
Topoisomerase I Inhibitors

Turmeric has antioxidant effects. There is some concern that this may reduce the activity of chemotherapy drugs that generate free radicals. However, research is conflicting.
In vitro research shows that curcumin, a constituent of turmeric, inhibits camptothecin-induced apoptosis of breast cancer cells by up to 71%. However, other in vitro research shows that curcumin augments the cytotoxic effects of camptothecin. Reasons for the discrepancies may relate to the dose of curcumin and the chemotherapeutic agents. Lower doses of curcumin might have antioxidant effects while higher doses might have pro-oxidant effects. More evidence is needed to determine what effect, if any, turmeric might have.

Likelihood Possible Evidence D
Tramadol (Ultram)

Theoretically, turmeric might increase or decrease levels of tramadol.
Animal research suggests that a single dose of curcumin, a constituent of turmeric, may increase tramadol's maximum concentration (Cmax) by inhibiting metabolism, while continued daily use for 7 days may reduce the area under the curve (AUC) due to the induction of drug-metabolizing enzymes such as cytochrome P450 3A4 (CYP3A4). However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Turmeric might increase the risk of bleeding with warfarin.
One case of increased international normalized ratio (INR) has been reported for a patient taking warfarin who began taking turmeric. Prior to taking turmeric, the patient had stable INR measurements. Within a few weeks of starting turmeric supplementation, the patient's INR increased to 10. Additionally, curcumin, the active constituent in turmeric, has demonstrated antiplatelet effects in vitro, which may produce additive effects when taken with warfarin.

Likelihood Possible Evidence D
Cytochrome P450 1A2 (Cyp1A2) Substrates

Theoretically, turmeric might increase levels of drugs metabolized by CYP1A2. However, research is conflicting.
In vitro and animal research show that the turmeric constituent, curcumin, inhibits CYP1A2. However, other in vitro research suggests that curcumin does not significantly affect CYP1A2.

Likelihood Possible Evidence D
Docetaxel (Taxotere)

Theoretically, turmeric might increase blood levels of oral docetaxel.
Animal research suggests that the turmeric constituent, curcumin, enhances the oral bioavailability of docetaxel. However, the significance of this interaction is unclear, as this drug is typically administered intravenously in clinical settings.

Likelihood Possible Evidence D
Estrogens

Theoretically, large amounts of turmeric might interfere with hormone replacement therapy through competition for estrogen receptors.
In vitro research shows that curcumin, a constituent of turmeric, displaces the binding of estrogen to its receptors.

Likelihood Possible Evidence D
Glyburide (Diabeta, Others)

Theoretically, taking turmeric and glyburide in combination might increase the risk of hypoglycemia.
Clinical research shows that taking curcumin 475 mg daily for 10 days prior to taking glyburide 5 mg increases blood levels of glyburide by 12% at 2 hours after the dose in patients with type 2 diabetes. While maximal blood concentrations of glyburide were not affected, turmeric modestly decreased postprandial glucose levels for up to 24 hours when compared to glyburide alone, possibly due to the hypoglycemic effect of turmeric demonstrated in animal research.

Likelihood Possible Evidence B
Losartan (Cozaar)

Theoretically, turmeric might increase the effects of losartan.
Research in hypertensive rats shows that taking turmeric can increase the hypotensive effects of losartan.

Likelihood Possible Evidence D
Norfloxacin (Noroxin)

Theoretically, turmeric might increase the effects and adverse effects of norfloxacin.
Animal research shows that taking curcumin, a turmeric constituent, can increase blood levels of orally administered norfloxacin.

Likelihood Possible Evidence D
P-Glycoprotein Substrates

Theoretically, turmeric might increase the absorption of P-glycoprotein substrates.
In vitro and animal research shows that curcuminoids and other constituents found in turmeric can inhibit P-glycoprotein expression and activity.

Likelihood Possible Evidence D
Paclitaxel (Abraxane, Onxol)

Theoretically, turmeric might alter blood levels of paclitaxel, although any effect may not be clinically relevant.
Clinical research in adults with breast cancer receiving intravenous paclitaxel suggests that taking turmeric may modestly alter paclitaxel pharmacokinetics. Patients received paclitaxel on day 1, followed by either no treatment or turmeric 2 grams daily from days 2-22. Pharmacokinetic modeling suggests that turmeric reduces the maximum concentration and area under the curve of paclitaxel by 12.1% and 7.7%, respectively. However, these changes are not likely to be considered clinically relevant. Conversely, animal research suggests that curcumin, a constituent of turmeric, enhances the oral bioavailability of paclitaxel. However, the significance of this interaction is unclear, as this drug is typically administered intravenously in clinical settings.

Likelihood Possible Evidence D
Turmeric full monograph & interactions

Chitraka10 drug types · 1,097 drugs

Anticoagulant/Antiplatelet Drugs

There is some concern that Ceylon leadwort might potentiate the effects of anticoagulant and antiplatelet drugs and possibly increase the risk of bleeding. Ceylon leadwort root extract has been shown to decrease platelet adhesion and prolong bleeding in animals. However, this effect has not yet been demonstrated in humans. Until more is known, use cautiously in patients taking anticoagulant or antiplatelet drugs. Some of these drugs include aspirin, clopidogrel (Plavix), dalteparin (Fragmin), enoxaparin (Lovenox), heparin, ticlopidine (Ticlid), warfarin (Coumadin), and others.

Likelihood Possible Evidence D
Antidiabetes Drugs

Ceylon leadwort root extract has been shown to both increase and decrease blood glucose levels in animal research. This effect has not yet been demonstrated in humans. Theoretically, Ceylon leadwort might reduce or potentiate the effects of antidiabetes drugs. Monitor blood glucose levels closely. Medication dose adjustments may be necessary. Some antidiabetes drugs include glimepiride (Amaryl), glyburide (Diabeta, Glynase PresTab, Micronase), insulin, pioglitazone (Actos), rosiglitazone (Avandia), and others.

Likelihood Possible Evidence D
Cytochrome P450 1A2 (Cyp1A2) Substrates

Plumbagin, a constituent of Ceylon leadwort, has been shown to inhibit cytochrome P450 1A2 (CYP1A2) in vitro. So far, this interaction has not been reported in humans. Theoretically, Ceylon leadwort might increase the levels of drugs metabolized by CYP1A2. Some substrates of CYP1A2 include clozapine (Clozaril), cyclobenzaprine (Flexeril), fluvoxamine (Luvox), haloperidol (Haldol), imipramine (Tofranil), mexiletine (Mexitil), olanzapine (Zyprexa), pentazocine (Talwin), propranolol (Inderal), tacrine (Cognex), zileuton (Zyflo), zolmitriptan (Zomig), and others.

Likelihood Possible Evidence D
Cytochrome P450 2B6 (Cyp2B6) Substrates

Plumbagin, a constituent of Ceylon leadwort, has been shown to inhibit cytochrome P450 2B6 (CYP2B6) in vitro. So far, this interaction has not been reported in humans. Theoretically, Ceylon leadwort might increase the levels of drugs metabolized by CYP2B6. Drugs that are metabolized by CYP2B6 include ketamine (Ketalar), phenobarbital, orphenadrine (Norflex), secobarbital (Seconal), and dexamethasone (Decadron).

Likelihood Possible Evidence D
Cytochrome P450 2C9 (Cyp2C9) Substrates

Plumbagin, a constituent of Ceylon leadwort, has been shown to inhibit cytochrome P450 2C9 (CYP2C9) in vitro. So far, this interaction has not been reported in humans. Theoretically, Ceylon leadwort might increase the levels of drugs metabolized by CYP2C9. Drugs that are metabolized by CYP2C9 include celecoxib (Celebrex), diclofenac (Voltaren), fluvastatin (Lescol), glipizide (Glucotrol), ibuprofen (Advil, Motrin), irbesartan (Avapro), losartan (Cozaar), phenytoin (Dilantin), piroxicam (Feldene), tamoxifen (Nolvadex), tolbutamide (Tolinase), torsemide (Demadex), and S-warfarin (Coumadin).

Likelihood Possible Evidence D
Cytochrome P450 2D6 (Cyp2D6) Substrates

Plumbagin, a constituent of Ceylon leadwort, has been shown to inhibit cytochrome P450 2D6 (CYP2D6) in vitro. So far, this interaction has not been reported in humans. Theoretically, Ceylon leadwort might increase the levels of drugs metabolized by CYP2D6. Some drugs metabolized by CYP2D6 include amitriptyline (Elavil), codeine, desipramine (Norpramin), flecainide (Tambocor), fluoxetine (Prozac), ondansetron (Zofran), tramadol (Ultram), and others.

Likelihood Possible Evidence D
Cytochrome P450 2E1 (Cyp2E1) Substrates

Plumbagin, a constituent of Ceylon leadwort, has been shown to inhibit cytochrome P450 2E1 (CYP2E1) in vitro. So far, this interaction has not been reported in humans. Theoretically, Ceylon leadwort might increase the levels of drugs metabolized by CYP2E1. Some drugs metabolized by CYP2E1 include acetaminophen, chlorzoxazone (Parafon Forte), ethanol, theophylline, and anesthetics such as enflurane (Ethrane), halothane (Fluothane), isoflurane (Forane), methoxyflurane (Penthrane).

Likelihood Possible Evidence D
Cytochrome P450 3A4 (Cyp3A4) Substrates

Plumbagin, a constituent of Ceylon leadwort, has been shown to inhibit cytochrome P450 3A4 (CYP3A4) in vitro. So far, this interaction has not been reported in humans. Theoretically, Ceylon leadwort might increase the levels of drugs metabolized by CYP3A4. Some drugs metabolized by CYP3A4 include lovastatin (Mevacor), clarithromycin (Biaxin), indinavir (Crixivan), sildenafil (Viagra), triazolam (Halcion), and numerous others.

Likelihood Possible Evidence D
Estrogens

Laboratory research suggests that Ceylon leadwort root extract has anti-estrogenic activity. Theoretically, Ceylon leadwort may interfere with hormone therapy.

Likelihood Possible Evidence D
Immunosuppressants

Plumbagin, a constituent of Ceylon leadwort, has demonstrated immunosuppressant activity in animal research. Theoretically, Ceylon leadwort might interfere with immunosuppressive therapy. Immunosuppressant drugs include azathioprine (Imuran), basiliximab (Simulect), cyclosporine (Neoral, Sandimmune), daclizumab (Zenapax), muromonab-CD3 (OKT3, Orthoclone OKT3), mycophenolate (CellCept), tacrolimus (FK506, Prograf), sirolimus (Rapamune), prednisone (Deltasone, Orasone), corticosteroids (glucocorticoids), and others.

Likelihood Possible Evidence D
Chitraka full monograph & interactions

Kali Mirch17 drug types · 1,019 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, black pepper might increase the risk of bleeding when taken with antiplatelet or anticoagulant drugs.
In vitro research shows that piperine, a constituent of black pepper, seems to inhibit platelet aggregation. This has not been reported in humans.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, black pepper might increase the risk of hypoglycemia when taken with antidiabetes drugs.
Animal research shows that piperine, a constituent of black pepper, can reduce blood glucose levels. Monitor blood glucose levels closely. Dose adjustments might be necessary.

Likelihood Possible Evidence D
Atorvastatin (Lipitor)

Theoretically, black pepper might increase blood levels of atorvastatin.
Animal research shows that taking piperine, a constituent of black pepper, 35 mg/kg can increase the maximum serum concentration of atorvastatin three-fold. This has not been reported in humans.

Likelihood Possible Evidence D
Cyclosporine (Neoral, Sandimmune)

Theoretically, black pepper might increase the effects and side effects of cyclosporine.
In vitro research shows that piperine, a constituent of black pepper, increases the bioavailability of cyclosporine. This has not been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 2D6 (Cyp2D6) Substrates

Theoretically, black pepper might increase levels of drugs metabolized by CYP2D6.
In vitro research suggests that some constituents of black pepper inhibit CYP2D6. This has not been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 3A4 (Cyp3A4) Substrates

Theoretically, black pepper might increase levels of drugs metabolized by CYP3A4.
In vitro research and pharmacokinetic simulation data suggest that piperine, a constituent of black pepper, as well as the pepper fruit seem to inhibit CYP3A4. This has not been reported in humans.

Likelihood Possible Evidence D
Lithium

Theoretically, black pepper might increase blood levels of lithium due to its diuretic effects. The dose of lithium might need to be reduced.
Black pepper is thought to have diuretic properties.

Likelihood Probable Evidence D
Nevirapine (Viramune)

Black pepper might increase blood levels of nevirapine.
Clinical research shows that piperine, a constituent of black pepper, increases the plasma concentration of nevirapine. However, no adverse effects were observed in this study.

Likelihood Probable Evidence D
P-Glycoprotein Substrates

Theoretically, black pepper might increase levels of P-glycoprotein substrates.
In vitro research shows that piperine, a constituent of black pepper, seems to inhibit P-glycoprotein.

Likelihood Possible Evidence D
Pentobarbital (Nembutal)

Theoretically, black pepper might increase the sedative effects of pentobarbital.
Animal research shows that piperine, a constituent of black pepper, increases pentobarbital-induced sleeping time.

Likelihood Possible Evidence D
Phenytoin (Dilantin)

Black pepper might increase blood levels of phenytoin.
Clinical research shows that piperine, a constituent of black pepper, seems to increase absorption, slow elimination, and increase levels of phenytoin. Taking a single dose of black pepper 1 gram along with phenytoin seems to double the serum concentration of phenytoin. Consuming a soup with black pepper providing piperine 44 mg/200 mL of soup along with phenytoin also seems to increase phenytoin levels when compared with consuming the same soup without black pepper.

Likelihood Possible Evidence B
Propranolol (Inderal)

Black pepper might increase blood levels of propranolol.
Clinical research shows that piperine, a constituent of black pepper, seems to increase absorption and slow elimination of propranolol.

Likelihood Possible Evidence B
Rifampin (Rifadin)

Black pepper might increase blood levels of rifampin.
Clinical research shows that piperine, a constituent of black pepper, seems to increase absorption and serum levels of rifampin.

Likelihood Possible Evidence B
Theophylline

Black pepper might increase blood levels of theophylline.
Clinical research shows that piperine, a constituent of black pepper, seems to increase absorption and slow elimination of theophylline.

Likelihood Possible Evidence D
Amoxicillin (Amoxil, Trimox)

Theoretically, black pepper might increase the effects and side effects of amoxicillin.
Animal research shows that taking piperine, a constituent of black pepper, with amoxicillin increases plasma levels of amoxicillin. This has not been reported in humans.

Likelihood Possible Evidence D
Carbamazepine (Tegretol)

Theoretically, black pepper might increase blood levels of carbamazepine, potentially increasing the effects and side effects of carbamazepine.
One clinical study in patients taking carbamazepine 300 mg or 500 mg twice daily shows that taking a single 20 mg dose of purified piperine, a constituent of black pepper, increases carbamazepine levels. Piperine may increase carbamazepine absorption by increasing blood flow to the GI tract, increasing the surface area of the small intestine, or inhibiting cytochrome P450 3A4 (CYP3A4) in the gut wall. Absorption was significantly increased by 7-10 mcg/mL/hour. The time to eliminate carbamazepine was also increased by 4-8 hours. Although carbamazepine levels were increased, this did not appear to increase side effects. In vitro research also shows that piperine can increase carbamazepine levels by 11% in a time-dependent manner.

Likelihood Possible Evidence B
Cytochrome P450 1A2 (Cyp1A2) Substrates

Theoretically, black pepper might decrease levels and clinical effects of drugs metabolized by CYP1A2.
In vitro research suggests that black pepper induces CYP1A2. This has not been reported in humans.

Likelihood Possible Evidence D
Kali Mirch full monograph & interactions

Sunthi14 drug types · 1,007 drugs

Anticoagulant/Antiplatelet Drugs

Ginger may have antiplatelet effects and may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs. However, research is conflicting.
Laboratory research suggests that ginger inhibits thromboxane synthetase and decreases platelet aggregation. However, this has not been demonstrated unequivocally in humans, with mixed results from clinical trials. Theoretically, excessive amounts of ginger might increase the risk of bleeding when used with anticoagulant/antiplatelet drugs.

Likelihood Possible Evidence B
Antidiabetes Drugs

Theoretically, taking ginger with antidiabetes drugs might increase the risk of hypoglycemia.
Animal and human research suggests that ginger might increase insulin levels and/or decrease blood glucose levels.

Likelihood Possible Evidence D
Cytochrome P450 3A4 (Cyp3A4) Substrates

Ginger might increase or decrease the levels of CYP3A4 substrates.
In vitro research and some case reports suggest that ginger inhibits CYP3A4 activity. Three case reports from the World Health Organization (WHO) adverse drug reaction database describe increased toxicity in patients taking ginger and cancer medications that are CYP3A4 substrates (imatinib, dabrafenib, and crizotinib). However, the causality of this interaction is unclear due to the presence of multiple interacting drugs and routes of administration.
Conversely, other in vitro research suggests that ginger induces CYP3A4 activity, leading to reduced levels of CYP3A4 substrates. However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Losartan (Cozaar)

Theoretically, ginger might increase levels of losartan and the risk of hypotension.
In animal research, ginger increased the levels and hypotensive effects of a single dose of losartan. It is not clear if ginger alters the concentration or effects of losartan when taken continuously. Additionally, this interaction has not been shown in humans.

Likelihood Possible Evidence D
Nifedipine (Procardia)

Ginger may have antiplatelet effects and increase the risk of bleeding if used with nifedipine.
Clinical research shows that combined treatment with ginger 1 gram plus nifedipine 10 mg significantly inhibits platelet aggregation when compared to nifedipine or ginger alone.

Likelihood Possible Evidence B
P-Glycoprotein Substrates

Ginger might increase the absorption and blood levels of P-glycoprotein (P-gp) substrates.
In vitro research and case reports suggest that ginger inhibits drug efflux by P-gp, potentially increasing absorption and serum levels of P-gp substrates. Two case reports from the World Health Organization (WHO) adverse drug reaction database describe increased toxicity in patients taking ginger and cancer medications that are P-gp substrates (trametinib, crizotinib). However, the causality of this interaction is unclear due to the presence of multiple interacting drugs and routes of administration.

Likelihood Possible Evidence D
Phenprocoumon (Marcoumar, Others)

Ginger might increase the risk of bleeding with phenprocoumon.
Phenprocoumon, a warfarin-related anticoagulant, might increase the international normalized ratio (INR) when taken with ginger. There is one case report of a 76-year-old woman with a stable INR on phenprocoumon that increased to greater than 10 when she began consuming dried ginger and ginger tea.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Ginger might increase the risk of bleeding with warfarin.
Laboratory research suggests that ginger might inhibit thromboxane synthetase and decrease platelet aggregation. In one case report, ginger increased the INR when taken with phenprocoumon, which has similar pharmacological effects as warfarin. In another case report, ginger increased the INR when taken with a combination of warfarin, hydrochlorothiazide, and acetaminophen. A longitudinal analysis suggests that taking ginger increases the risk of bleeding in patients taking warfarin for at least 4 months. However, research in healthy people suggests that ginger has no effect on INR, or the pharmacokinetics or pharmacodynamics of warfarin. Until more is known, monitor INRs closely in patients taking large amounts of ginger.

Likelihood Possible Evidence B
Calcium Channel Blockers

Theoretically, taking ginger with calcium channel blockers might increase the risk of hypotension.
Some animal and in vitro research suggests that ginger has hypotensive and calcium channel-blocking effects. Another animal study shows that concomitant administration of ginger and the calcium channel blocker amlodipine leads to greater reductions in blood pressure when compared with amlodipine alone.

Likelihood Unlikely Evidence D
Cyclosporine (Neoral, Sandimmune)

Theoretically, when taken prior to cyclosporine, ginger might decrease cyclosporine levels.
In an animal model, ginger juice taken 2 hours prior to cyclosporine administration reduced the maximum concentration and area under the curve of cyclosporine by 51% and 40%, respectively. This effect was not observed when ginger juice and cyclosporine were administered at the same time.

Likelihood Possible Evidence D
Cytochrome P450 1A2 (Cyp1A2) Substrates

Theoretically, ginger might increase the levels of CYP1A2 substrates.
In vitro research shows that ginger inhibits CYP1A2 activity. However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 2B6 (Cyp2B6) Substrates

Theoretically, ginger might increase the levels of CYP2B6 substrates.
In vitro research shows that ginger inhibits CYP2B6 activity. However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 2C9 (Cyp2C9) Substrates

Theoretically, ginger might increase the levels of CYP2C9 substrates.
In vitro research shows that ginger inhibits CYP2C9 activity. However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Metronidazole (Flagyl)

Theoretically, ginger might increase levels of metronidazole.
In an animal model, ginger increased the absorption and plasma half-life of metronidazole. In addition, the elimination rate and clearance of metronidazole was significantly reduced.

Likelihood Possible Evidence D
Sunthi full monograph & interactions

Baheda7 drug types · 933 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, concomitant use of Terminalia arjuna with anticoagulant or antiplatelet drugs may increase the risk of bleeding in some patients.
In vitro, Terminalia arjuna bark extract inhibits platelet aggregation, decreases platelet activation, and shows antithrombotic properties.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, concomitant use of Terminalia bellirica or Terminalia chebula with antidiabetes drugs could affect blood sugar control and increase the risk of hypoglycemia.
Animal and in vitro research shows that Terminalia bellirica and Terminalia chebula fruit and seed extract have hypoglycemic effects.

Likelihood Possible Evidence D
Chlorzoxazone (Parafon Forte, Paraflex)

Theoretically, use of Terminalia chebula may increase the risk of adverse effects from chlorzoxazone.
Animal research shows that enteral administration of Terminalia chebula for 15 days prior to administration of chlorzoxazone increases blood levels of chlorzoxazone and decreases chlorzoxazone clearance. It is speculated that Terminalia chebula reduces the metabolism of chlorzoxazone by inhibiting cytochrome P450 2E1.

Likelihood Possible Evidence D
Cytochrome P450 2C9 (Cyp2C9) Substrates

Theoretically, use of Terminalia arjuna may increase the levels and clinical effects of CYP2C9 substrates.
In vitro research shows that Terminalia arjuna extract inhibits CYP2C9 enzymes and reduces CYP2C9 substrate metabolism.

Likelihood Possible Evidence D
Cytochrome P450 2D6 (Cyp2D6) Substrates

Theoretically, use of Terminalia arjuna may increase the levels and clinical effects of CYP2D6 substrates.
In vitro research shows that Terminalia arjuna extract inhibits CYP2D6 enzymes and reduces CYP2D6 substrate metabolism.

Likelihood Possible Evidence D
Cytochrome P450 3A4 (Cyp3A4) Substrates

Theoretically, use of Terminalia arjuna may increase the levels and clinical effects of CYP3A4 substrates.
In vitro research shows that Terminalia arjuna extract inhibits CYP3A4 enzymes and reduces CYP3A4 substrate metabolism.

Likelihood Possible Evidence D
Omeprazole (Prilosec)

Theoretically, use of Terminalia chebula may increase the risk of adverse effects from omeprazole.
Animal research shows that enteral administration of Terminalia chebula for 15 days prior to administration of omeprazole increases blood levels of omeprazole and decreases omeprazole clearance. It is speculated that Terminalia chebula reduces the metabolism of omeprazole by inhibiting cytochrome P450 2C19.

Likelihood Possible Evidence D
Baheda full monograph & interactions

Pippali14 drug types · 896 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, Indian long pepper might increase the risk of bleeding when taken with anticoagulant/antiplatelet drugs.
In vitro research shows that Indian long pepper extract inhibits platelet aggregation.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, Indian long pepper might increase the risk of hypoglycemia when taken with antidiabetes drugs.
Animal research shows that piperine, a constituent of Indian long pepper, can reduce blood glucose levels. Monitor blood glucose levels closely. Dose adjustments might be necessary.

Likelihood Possible Evidence D
Cyclosporine (Neoral, Sandimmune)

Theoretically, Indian long pepper might increase the effects and adverse effects of cyclosporine.
In vitro research shows that piperine, a constituent of Indian long pepper, increases the bioavailability of cyclosporine.

Likelihood Possible Evidence D
Cytochrome P450 3A4 (Cyp3A4) Substrates

Theoretically, Indian long pepper might increase the effects and adverse effects of CYP3A4 substrates.
In vitro research shows that piperine, a constituent of Indian long pepper, inhibits CYP3A4.

Likelihood Possible Evidence D
Nevirapine (Viramune)

Theoretically, Indian long pepper might increase blood levels of nevirapine.
A small pharmacokinetic study shows that piperine, a constituent of Indian long pepper, increases the plasma concentration and systemic exposure of nevirapine. However, no adverse effects were associated with the elevated plasma levels of nevirapine.

Likelihood Probable Evidence B
P-Glycoprotein Substrates

Theoretically, Indian long pepper might increase levels of P-glycoprotein substrates.
In vitro research shows that piperine, a constituent of Indian long pepper, can inhibit P-glycoprotein.

Likelihood Possible Evidence D
Pentobarbital (Nembutal)

Theoretically, Indian long pepper might increase the sedative effects of pentobarbital.
Animal research shows that piperine, a constituent of Indian long pepper, can increase pentobarbitone-induced sleeping time.

Likelihood Possible Evidence D
Phenytoin (Dilantin)

Theoretically, Indian long pepper might increase blood levels of phenytoin.
A small pharmacokinetic study shows that piperine, a constituent of Indian long pepper, increases phenytoin serum levels and slows its elimination.

Likelihood Possible Evidence B
Propranolol (Inderal)

Theoretically, Indian long pepper might increase blood levels of propranolol.
A small pharmacokinetic study shows that piperine, a constituent of Indian long pepper, accelerates absorption and increases serum concentrations of propranolol.

Likelihood Possible Evidence B
Rifampin (Rifadin)

Theoretically, Indian long pepper might increase blood levels of rifampin.
Piperine, a constituent of Indian long pepper, seems to increase absorption and serum levels of rifampin.

Likelihood Possible Evidence D
Theophylline

Indian long pepper might increase blood levels of theophylline.
A small pharmacokinetic study shows that piperine, a constituent of Indian long pepper, increases serum concentrations and slows elimination of theophylline.

Likelihood Possible Evidence B
Amoxicillin (Amoxil, Trimox)

Theoretically, Indian long pepper might increase the effects and adverse effects of amoxicillin.
Evidence from animal research shows that piperine, a constituent of Indian long pepper, increases the plasma levels of amoxicillin when taken concomitantly.

Likelihood Possible Evidence D
Carbamazepine (Tegretol)

Theoretically, Indian long pepper might increase blood levels of carbamazepine.
A small pharmacokinetic study in patients taking carbamazepine 300 mg or 500 mg twice daily shows that a single 20 mg dose of purified piperine, which is a constituent of Indian long pepper, increases carbamazepine levels. Piperine may increase absorption by increasing blood flow to the GI tract, increasing the surface area of the small intestine, or by cytochrome P450 3A4 (CYP3A4) inhibition in the gut wall. Absorption was significantly increased by 7-10 mcg/mL/hour. The time to eliminate carbamazepine was also increased by 4-8 hours. Although carbamazepine levels were increased, this did not appear to increase side effects.

Likelihood Possible Evidence B
Cefotaxime (Claforan)

Theoretically, Indian long pepper might increase the effects and adverse effects of cefotaxime.
Animal research shows that piperine, a constituent of Indian long pepper, increases the plasma levels of cefotaxime when taken concomitantly.

Likelihood Possible Evidence D
Pippali full monograph & interactions

Giloy6 drug types · 612 drugs

Antidiabetes Drugs

Theoretically, Tinospora cordifolia might increase the risk of hypoglycemia when taken with antidiabetes drugs.
Clinical research in adults with type 2 diabetes shows that Tinospora cordifolia can reduce fasting blood glucose and glycated hemoglobin. Additionally, animal research shows that Tinospora cordifolia has hypoglycemic effects.

Likelihood Possible Evidence A
Cytochrome P450 1A2 (Cyp1A2) Substrates

Theoretically, Tinospora cordifolia might increase levels of drugs metabolized by CYP1A2.
In vitro research shows that Tinospora cordifolia extract inhibits CYP1A2 at high concentrations. However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 2C19 (Cyp2C19) Substrates

Theoretically, Tinospora cordifolia might increase levels of drugs metabolized by CYP2C19.
In vitro research shows that Tinospora cordifolia extract inhibits CYP2C19 at high concentrations. However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 2C9 (Cyp2C9) Substrates

Theoretically, Tinospora cordifolia might increase levels of drugs metabolized by CYP2C9.
In vitro research shows that Tinospora cordifolia extract inhibits CYP2C9. Animal research shows that Tinospora cordifolia extract 400 mg/kg twice daily for 14 days reduces the clearance and increases plasma levels of glyburide, a CYP2C9 substrate. However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 2D6 (Cyp2D6) Substrates

Theoretically, Tinospora cordifolia might increase levels of drugs metabolized by CYP2D6.
In vitro research shows that Tinospora cordifolia extract inhibits CYP2D6 at high concentrations. However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Immunosuppressants

Theoretically, Tinospora cordifolia might reduce the effectiveness of immunosuppressants.
In vitro and animal research shows that Tinospora cordifolia has immunostimulant effects.

Likelihood Possible Evidence D
Giloy full monograph & interactions

Kalmegh6 drug types · 413 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, andrographis might increase the risk of bleeding when used with anticoagulant or antiplatelet drugs.
Animal and laboratory studies suggest that andrographis has antiplatelet effects.

Likelihood Possible Evidence D
Antihypertensive Drugs

Theoretically, andrographis might increase the risk of hypotension when used with antihypertensive drugs.
Animal research suggests that andrographis has hypotensive effects.

Likelihood Possible Evidence D
Immunosuppressants

Theoretically, andrographis might interfere with the effects of immunosuppressive drugs.
Laboratory research suggests that andrographolide has immunostimulant activity.

Likelihood Possible Evidence D
Celecoxib (Celebrex)

Theoretically, andrographis extract might increase the maximum concentration and time to peak concentration of celecoxib. The clinical significance of these changes is unclear.
Animal research suggests that andrographis extract taken orally increases the maximum concentration and time to peak concentration of celecoxib but does not appear to impact the area under the curve.

Likelihood Possible Evidence D
Etoricoxib (Arcoxia)

Theoretically, andrographis might decrease the absorption of etoricoxib, although the clinical significance is unclear.
Animal research shows that andrographis extract, or the constituent andrographolide, taken orally with etoricoxib decreases the bioavailability of etoricoxib. However, this reduced bioavailability is not correlated with a reduction in the anti-inflammatory effects of etoricoxib in arthritic mice models. The clinical significance of this interaction is unclear.

Likelihood Possible Evidence D
Glipizide (Glucotrol)

Theoretically, andrographis extract might increase the maximum concentration and area under the curve of glipizide; however, opposite effects are seen with the constituent, andrographolide. The clinical significance of this interaction is unclear.
Animal research suggests that andrographis extract taken orally with glipizide in diabetes-induced rats increases the maximum concentration and area under the curve of glipizide. However, the opposite effect is seen with the constituent, andrographolide, in which the maximum concentration and area under the curve are decreased when taken with glipizide.

Likelihood Possible Evidence D
Kalmegh full monograph & interactions

Magnesium Stearate15 drug types · 295 drugs

Levodopa/Carbidopa (Sinemet)

Magnesium can reduce the bioavailability of levodopa/carbidopa.
Clinical research in healthy volunteers shows that taking magnesium oxide 1000 mg with levodopa 100 mg/carbidopa 10 mg reduces the area under the curve (AUC) of levodopa by 35% and of carbidopa by 81%. In vitro and animal research shows that magnesium produces an alkaline environment in the digestive tract, which might lead to degradation and reduced bioavailability of levodopa/carbidopa.

Likelihood Probable Evidence B
Aminoglycoside Antibiotics

Concomitant use of aminoglycoside antibiotics and magnesium can increase the risk for neuromuscular weakness.
Both aminoglycosides and magnesium reduce presynaptic acetylcholine release, which can lead to neuromuscular blockade and possible paralysis. This is most likely to occur with high doses of magnesium given intravenously.

Likelihood Possible Evidence D
Antacids

Use of acid reducers may reduce the laxative effect of magnesium oxide.
A retrospective analysis shows that, in the presence of H2 receptor antagonists (H2RAs) or proton pump inhibitors (PPIs), a higher dose of magnesium oxide is needed for a laxative effect. This may also occur with antacids. Under acidic conditions, magnesium oxide is converted to magnesium chloride and then to magnesium bicarbonate, which has an osmotic laxative effect. By reducing acidity, antacids may reduce the conversion of magnesium oxide to the active bicarbonate salt.

Likelihood Possible Evidence D
Bictegravir/Emtricitabine/Tenofovir Alafenamide (Biktarvy)

Magnesium might decrease levels of bictegravir/emtricitabine/tenofovir alafenamide by reducing its absorption.
Advise patients that bictegravir/emtricitabine/tenofovir alafenamide should be taken at least 2 hours before or 6 hours after magnesium containing products.

Likelihood Probable Evidence D
Bisphosphonates

Magnesium can decrease absorption of bisphosphonates.
Cations, including magnesium, can decrease bisphosphonate absorption. Advise patients to separate doses of magnesium and these drugs by at least 2 hours.

Likelihood Probable Evidence B
Calcium Channel Blockers

Magnesium can have additive effects with calcium channel blockers, although evidence is conflicting.
Magnesium inhibits calcium entry into smooth muscle cells and may therefore have additive effects with calcium channel blockers. Severe hypotension and neuromuscular blockades may occur when nifedipine is used with intravenous magnesium, although some contradictory evidence suggests that concurrent use of magnesium with nifedipine does not increase the risk of neuromuscular weakness. High doses of magnesium could theoretically have additive effects with other calcium channel blockers.

Likelihood Possible Evidence D
Digoxin

Magnesium salts may reduce absorption of digoxin.
Clinical evidence suggests that treatment with oral magnesium hydroxide or magnesium trisilicate reduces absorption of digoxin from the intestines. This may reduce the blood levels of digoxin and decrease its therapeutic effects.

Likelihood Possible Evidence B
Potassium-Sparing Diuretics

Potassium-sparing diuretics decrease excretion of magnesium, possibly increasing magnesium levels.
Potassium-sparing diuretics also have magnesium-sparing properties, which can counteract the magnesium losses associated with loop and thiazide diuretics. Theoretically, increased magnesium levels could result from concomitant use of potassium-sparing diuretics and magnesium supplements.

Likelihood Probable Evidence D
Quinolone Antibiotics

Magnesium decreases absorption of quinolones.
Magnesium can form insoluble complexes with quinolones and decrease their absorption. Advise patients to take these drugs at least 2 hours before, or 4 to 6 hours after, magnesium supplements.

Likelihood Probable Evidence D
Skeletal Muscle Relaxants

Parenteral magnesium alters the pharmacokinetics of skeletal muscle relaxants, increasing their effects and accelerating the onset of effect.
Parenteral magnesium shortens the time to onset of skeletal muscle relaxants by about 1 minute and prolongs the duration of action by about 2 minutes. Magnesium potentiates the effects of skeletal muscle relaxants by decreasing calcium-mediated release of acetylcholine from presynaptic nerve terminals, reducing postsynaptic sensitivity to acetylcholine, and having a direct effect on the membrane potential of myocytes. Magnesium also has vasodilatory actions and increases cardiac output, allowing a greater amount of muscle relaxant to reach the motor end plate. A clinical study found that low-dose rocuronium (0.45 mg/kg), when given after administration of magnesium 30 mg/kg over 10 minutes, has an accelerated onset of effect, which matches the onset of effect seen with a full-dose rocuronium regimen (0.6 mg/kg). In another clinical study, onset times for rocuronium doses of 0.3, 0.6, and 1.2 mg/kg were 86, 76, and 50 seconds, respectively, when given alone, but were reduced to 66, 44, and 38 seconds, respectively, when the doses were given after a 15-minute infusion of magnesium sulfate 60 mg/kg. Giving intraoperative intravenous magnesium sulfate, 50 mg/kg loading dose followed by 15 mg/kg/hour, reduces the onset time of rocuronium, enhances its clinical effects, reduces the dose of intraoperative opiates, and prolongs the spontaneous recovery time. It does not affect the activity of subsequently administered neostigmine.

Likelihood Probable Evidence A
Sulfonylureas

Magnesium increases the systemic absorption of sulfonylureas, increasing their effects and side effects.
Clinical research shows that administration of magnesium hydroxide with glyburide increases glyburide absorption, increases maximal insulin response by 35-fold, and increases the risk of hypoglycemia, when compared with glyburide alone. A similar interaction occurs between magnesium hydroxide and glipizide. The mechanism of this effect appears to be related to the elevation of gastrointestinal pH by magnesium-based antacids, increasing solubility and enhancing absorption of sulfonylureas.

Likelihood Probable Evidence B
Tetracycline Antibiotics

Magnesium decreases absorption of tetracyclines.
Magnesium can form insoluble complexes with tetracyclines in the gut and decrease their absorption and antibacterial activity. Advise patients to take these drugs 1 hour before or 2 hours after magnesium supplements.

Likelihood Probable Evidence D
Anticoagulant/Antiplatelet Drugs

Theoretically, magnesium may have antiplatelet effects, but the evidence is conflicting.
In vitro evidence shows that magnesium sulfate inhibits platelet aggregation, even at low concentrations. Some preliminary clinical evidence shows that infusion of magnesium sulfate increases bleeding time by 48% and reduces platelet activity. However, other clinical research shows that magnesium does not affect platelet aggregation, although inhibition of platelet-dependent thrombosis can occur.

Likelihood Unlikely Evidence B
Gabapentin (Neurontin)

Gabapentin absorption can be decreased by magnesium.
Clinical research shows that giving magnesium oxide orally along with gabapentin decreases the maximum plasma concentration of gabapentin by 33%, time to maximum concentration by 36%, and area under the curve by 43%. Advise patients to take gabapentin at least 2 hours before, or 4 to 6 hours after, magnesium supplements.

Likelihood Unlikely Evidence B
Sevelamer (Renagel, Renvela)

Sevelamer may increase serum magnesium levels.
In patients on hemodialysis, sevelamer use was associated with a 0.28 mg/dL increase in serum magnesium. The mechanism of this interaction remains unclear.

Likelihood Possible Evidence B
Magnesium Stearate full monograph & interactions

Ativisha2 drug types · 278 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, combining aconite with other antiplatelet or anticoagulant drugs might increase the risk of bruising and bleeding.
Higenamine, a constituent of aconite, is thought to have antiplatelet and antithrombotic effects. In an animal model of thrombosis, higenamine inhibited platelet aggregation and reduced the size of thrombus formation.

Likelihood Possible Evidence D
Stimulant Drugs

Theoretically, combining aconite with other stimulant drugs might alter the effects of the stimulant drug or increase the risk of cardiovascular toxicity.
Aconite and its constituents have stimulant effects due to agonist activity at beta-2-adrenoreceptors. In cardiac muscle, aconite appears to have a positive inotropic effect and increases heart rate and blood pressure. However, some constituents of aconite can reduce heart rate and blood pressure.

Likelihood Possible Evidence D
Ativisha full monograph & interactions

Dalchini2 drug types · 258 drugs

Antidiabetes Drugs

Theoretically, Ceylon cinnamon may have additive effects with antidiabetes drugs.
Ceylon cinnamon may lower blood glucose levels. Dose adjustments might be necessary.

Likelihood Possible Evidence D
Antihypertensive Drugs

Theoretically, Ceylon cinnamon might have additive effects with antihypertensive drugs and increase the risk of hypotension.
Animal research shows that Ceylon cinnamon extract has vasorelaxant properties and reduces blood pressure in rat models of hypertension, possibly via inhibition of calcium influx through L-type voltage-sensitive channels.

Likelihood Possible Evidence D
Dalchini full monograph & interactions

Amla4 drug types · 208 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, Indian gooseberry may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs; however, research is conflicting.
Clinical research shows that taking Indian gooseberry 500 mg as a single dose or twice daily for 10 days reduces platelet aggregation by about 24% to 36%, increases bleeding time by about 3.8-5.9 seconds, and increases clotting time by about 9.8-12.7 seconds when compared to baseline. However, taking Indian gooseberry 500 mg along with clopidogrel 75 mg or ecosprin 75 mg, as a single dose or for 10 days, does not significantly reduce platelet aggregation or increase bleeding time or clotting time when compared with clopidogrel 75 mg or ecosprin 75 mg alone. Until more is known, use caution when taking Indian gooseberry in combination with anticoagulant/antiplatelet drugs.

Likelihood Possible Evidence B
Antidiabetes Drugs

Taking Indian gooseberry with antidiabetes drugs might increase the risk of hypoglycemia.
Clinical research shows that taking Indian gooseberry fruit or fruit extract alone or in conjunction with antidiabetes medications can lower blood glucose levels. Dose adjustments to diabetes medications might be necessary.

Likelihood Possible Evidence B
Aspirin

Theoretically, Indian gooseberry may increase the risk of bleeding if used with aspirin; however, research is conflicting.
Clinical research shows that taking Indian gooseberry 500 mg as a single dose or twice daily for 10 days reduces platelet aggregation by about 24% to 36%, increases bleeding time by about 3.8-5.9 seconds, and increases clotting time by about 9.8-12.7 seconds when compared to baseline. However, taking a single dose of Indian gooseberry 500 mg along with ecosprin 75 mg, or taking a combination of Indian gooseberry 500 mg twice daily plus ecosprin 75 mg once daily for 10 days, does not significantly reduce platelet aggregation or increase bleeding time or clotting time when compared with ecosprin 75 mg alone.

Likelihood Possible Evidence B
Clopidogrel (Plavix)

Theoretically, Indian gooseberry may increase the risk of bleeding if used with clopidogrel; however, research is conflicting.
Clinical research shows that taking Indian gooseberry 500 mg as a single dose or twice daily for 10 days reduces platelet aggregation by about 24% to 36%, increases bleeding time by about 3.8-5.9 seconds, and increases clotting time by about 9.8-12.7 seconds when compared to baseline. However, taking a single dose of Indian gooseberry 500 mg along with clopidogrel 75 mg, or taking a combination of Indian gooseberry 500 mg twice daily plus clopidogrel 75 mg once daily for 10 days, does not significantly reduce platelet aggregation or increase bleeding time or clotting time when compared with clopidogrel 75 mg alone.

Likelihood Possible Evidence B
Amla full monograph & interactions

Sodium Starch Glycolate7 drug types · 205 drugs

Antihypertensive Drugs

Theoretically, a high intake of dietary sodium might reduce the effectiveness of antihypertensive drugs.
High intake of dietary sodium can increase systolic and diastolic blood pressure. Also, high intake of sodium may necessitate increased use of antihypertensive medications to achieve blood pressure control in some patients, such as those with chronic kidney disease.

Likelihood Probable Evidence A
Corticosteroids

Concomitant use of mineralocorticoids and some glucocorticoids with sodium supplements might increase the risk of hypernatremia.
Mineralocorticoids and some glucocorticoids (corticosteroids) cause sodium retention. This effect is dose-related and depends on mineralocorticoid potency. It is most common with hydrocortisone, cortisone, and fludrocortisone, followed by prednisone and prednisolone.

Likelihood Possible Evidence D
Didanosine (Videx)

Concomitant use of didanosine with additional sodium from dietary or supplemental sources may increase the risk of hypernatremia.
Didanosine formulations contain a significant amount of sodium.

Likelihood Probable Evidence C
Lithium

Altering dietary intake of sodium might alter the levels and clinical effects of lithium.
High sodium intake can reduce plasma concentrations of lithium by increasing lithium excretion. Reducing sodium intake can significantly increase plasma concentrations of lithium and cause lithium toxicity in patients being treated with lithium carbonate. Stabilizing sodium intake is shown to reduce the percentage of patients with lithium level fluctuations above 0.8 mEq/L. Patients taking lithium should avoid significant alterations in their dietary intake of sodium.

Likelihood Probable Evidence B
Sodium Phosphates

Theoretically, concomitant use of sodium phosphate with sodium supplements might increase the risk of hypernatremia.
Use of high doses (> 45 mL in 24 hours) of sodium phosphate, such as those used for bowel cleansing before surgery, can lead to serious electrolyte disturbances, including hypernatremia. The risk of hypernatremia is highest in the elderly and people with other risk factors for electrolyte disturbances.

Likelihood Possible Evidence D
Sodium-Containing Drugs

Concomitant use of sodium-containing drugs with additional sodium from dietary or supplemental sources may increase the risk of hypernatremia and long-term sodium-related complications.
The Chronic Disease Risk Reduction (CDRR) intake level of 2.3 grams of sodium daily indicates the intake at which it is believed that chronic disease risk increases for the apparently healthy population. Some medications contain high quantities of sodium. When used in conjunction with sodium supplements or high-sodium diets, the CDRR may be exceeded. Additionally, concomitant use may increase the risk for hypernatremia; this risk is highest in the elderly and people with other risk factors for electrolyte disturbances.

Likelihood Possible Evidence D
Tolvaptan (Samsca)

Theoretically, concomitant use of tolvaptan with sodium might increase the risk of hypernatremia.
Tolvaptan is a vasopressin receptor 2 antagonist that is used to increase sodium levels in patients with hyponatremia. Patients taking tolvaptan should use caution with the use of sodium salts such as sodium chloride.

Likelihood Probable Evidence C
Sodium Starch Glycolate full monograph & interactions

Shilajit Extract, Dry1 drug type · 86 drugs

Antidiabetes Drugs

Taking shilajit with antidiabetes drugs might increase the risk of hypoglycemia.
Most human and animal research shows that shilajit can decrease fasting plasma glucose levels. In an animal model, shilajit 100 mg per kg daily enhanced the glucose-lowering ability of both glibenclamide and metformin when given in combination over a 4 week period. Monitor blood glucose levels closely. Dose adjustments might be necessary.

Likelihood Possible Evidence D
Shilajit Extract, Dry full monograph & interactions
The maker

Brand information

Manufacturer and brand details for Chandraprabha Vati Tablet, from the product label.

Vedic Supplements

See all Vedic Supplements products
Name
Sumitra Remedies LLC
City
New Brunswick
State
NJ
ZipCode
08901
Phone Number
1-612-888-3342
Web Address
www.TheVedicStore.com
Pharmacist Counseling Corner

Chandraprabha Vati Tablet by Vedic Supplements: Common Questions

Does Chandraprabha Vati Tablet by Vedic Supplements interact with any medications?
Yes. Based on its ingredients, Chandraprabha Vati Tablet has a known interaction with 1,619 medications, including 8 rated major. Use the checker to see how it interacts with a specific drug.
How can one product interact with so many drugs?
Chandraprabha Vati Tablet contains 42 active ingredients, and an interaction can come from any of them. We check every ingredient, combine the results into one list per medication, and show which ingredient and mechanism is responsible.
Where does this information come from?
The product label data comes from the NIH Dietary Supplement Label Database (DSLD); the interaction data is built on the Natural Medicines database and reviewed by HelloPharmacist pharmacists.
Is this safe to take if I'm pregnant?
Several ingredients have safety concerns in pregnancy. Pippali and Pippali Mool are traditionally discouraged in medicinal amounts during pregnancy. Andrographis is rated possibly unsafe. Daru Haldi and Chitraka are likely unsafe. Ginger is often used for morning sickness, but check with your doctor first and keep amounts moderate. Other ingredients lack sufficient pregnancy data. Talk to your doctor or pharmacist about whether this product is safe for you personally.
Can I take this while breastfeeding?
Most ingredients lack reliable safety data for breastfeeding. Pippali, Pippali Mool, Andrographis, Tinospora cordifolia, Daru Haldi, and Chitraka should be avoided while nursing due to insufficient safety information or theoretical harm. Ginger is rated likely safe, and turmeric is likely safe. Check with your doctor or pharmacist before taking this product.
What is Tinospora cordifolia (Giloy) in this product supposed to do?
Tinospora cordifolia is possibly effective for type 2 diabetes and may help lower blood sugar. However, it has been linked to liver injury in some case reports, so it should be used carefully and under medical guidance.
Does this product have any fillers or inactive ingredients?
The product facts show there are no inactive ingredients listed for this formulation, meaning all the ingredients listed are active components of the Ayurvedic blend.
Can this help my high cholesterol?
Turmeric, one ingredient in this product, is possibly effective for high cholesterol. However, the effectiveness of the product as a whole hasn't been established, and it's not designed specifically for cholesterol. Talk to your doctor about whether this is appropriate for your condition.
I take blood pressure medication. Is this safe for me?
No—several ingredients in this product interact with blood pressure medications at Moderate severity, including magnesium, sodium starch glycolate, and others. Do not start this product without checking your specific medications with your pharmacist first.

Written and reviewed by the HelloPharmacist editorial staff. Our editorial policy

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Chandraprabha Vati Tablet label
Go deeper

The Full Monographs Behind Chandraprabha Vati Tablet’s Ingredients

Every ingredient we hold a full HelloPharmacist monograph for — uses, evidence, safety, and the complete interaction list.

Herb & supplement monograph

Magnesium

Interacts with 295 drugs

Magnesium is an essential mineral your body needs for muscles, nerves, blood pressure, and many other functions, and supplements are useful for preventing or correcting deficiency. Some othe...

Read the full Magnesium monograph → Herb & supplement monograph

Sodium

Interacts with 205 drugs

Sodium is an essential mineral and electrolyte your body needs to balance fluids, support nerves, and help muscles work. Most people in modern diets get more than enough—often too much—from...

Read the full Sodium monograph → Herb & supplement monograph

Indian Long Pepper

Interacts with 896 drugs

Indian long pepper (pippali) is a spice long used in Ayurvedic medicine and is best known for its piperine content, which may increase how well the body absorbs certain other substances. Mod...

Read the full Indian Long Pepper monograph → Herb & supplement monograph

Ginger

Interacts with 1,007 drugs

Ginger is a widely used culinary spice with a long history in traditional medicine, and it has the strongest evidence for helping with nausea and vomiting, including from motion sickness, pr...

Read the full Ginger monograph → Herb & supplement monograph

Andrographis

Interacts with 413 drugs

Andrographis is a bitter Asian herb traditionally used for colds, flu, and infections, and some studies suggest it may ease cold symptoms and shorten how long they last. The evidence is limi...

Read the full Andrographis monograph → Herb & supplement monograph

Tinospora Cordifolia

Interacts with 612 drugs

Tinospora cordifolia, known as Guduchi or Giloy in Ayurvedic medicine, is a climbing plant traditionally used to support immunity and treat fevers. Early laboratory and small human studies s...

Read the full Tinospora Cordifolia monograph → Herb & supplement monograph

Turmeric

Interacts with 1,133 drugs

Turmeric is a popular spice whose main active compounds, curcuminoids, are studied mostly for inflammation and joint pain. Some research is promising, but quality is mixed and curcumin is po...

Read the full Turmeric monograph → Herb & supplement monograph

Aconite

Interacts with 278 drugs

Aconite is a highly poisonous plant, and even small amounts of the raw or improperly processed root can cause severe, life-threatening reactions. There is no good scientific evidence that it...

Read the full Aconite monograph → Herb & supplement monograph

Tree Turmeric

Interacts with 1,160 drugs

Tree turmeric (Berberis aristata) is a shrub used in traditional Indian (Ayurvedic) medicine, valued mainly for its berberine content. Early research suggests possible benefits for blood sug...

Read the full Tree Turmeric monograph → Herb & supplement monograph

Ceylon Leadwort

Interacts with 1,097 drugs

Ceylon Leadwort (Plumbago zeylanica) is a plant long used in Ayurvedic and other traditional medicine systems, mainly for digestion, skin problems, and pain. Solid human studies are lacking,...

Read the full Ceylon Leadwort monograph → Herb & supplement monograph

Ceylon Cinnamon

Interacts with 258 drugs

Ceylon cinnamon is the so-called 'true' cinnamon, valued as a spice and used in traditional medicine for blood sugar, cholesterol, and digestion. Evidence for most health benefits is limited...

Read the full Ceylon Cinnamon monograph → Herb & supplement monograph

Terminalia

Interacts with 933 drugs

Terminalia is a group of traditional Ayurvedic tree species (most notably Terminalia arjuna) used for heart, digestive, and general wellness purposes. Some small studies suggest possible ben...

Read the full Terminalia monograph → Herb & supplement monograph

Indian Gooseberry

Interacts with 208 drugs

Indian gooseberry (amla) is a vitamin C-rich fruit used in Ayurvedic medicine for many purposes, from antioxidant support to cholesterol and digestion. Early research is promising for some u...

Read the full Indian Gooseberry monograph → Herb & supplement monograph

Black Pepper

Interacts with 1,019 drugs

Black pepper is a common kitchen spice that is generally safe in the amounts used in food. Its extract, piperine, is mostly added to supplements to help the body absorb other ingredients (li...

Read the full Black Pepper monograph → Herb & supplement monograph

Shilajit

Interacts with 86 drugs

Shilajit is a sticky, tar-like substance found in rocks of mountain ranges like the Himalayas, used in traditional Ayurvedic medicine for energy and vitality. Human evidence is limited and m...

Read the full Shilajit monograph → Herb & supplement monograph

Silicon

Silicon is a trace mineral found in the body and in foods like oats, barley, and certain fruits and vegetables, and it is popular in supplements for hair, skin, nail, and bone health. Some s...

Read the full Silicon monograph →
Sources

Sources & How We Checked

Chandraprabha Vati Tablet's label data comes from the NIH Dietary Supplement Label Database; the ingredient interaction data is from the Natural Medicines database, reviewed by our pharmacists.

Content is written and reviewed by licensed HelloPharmacist pharmacists. See our data sources and editorial standards for how this information is built and checked.

The 501 references behind this product’s interaction data

Every citation that drives the interaction findings for this product’s ingredients, from the evidence-graded Natural Medicines (TRC Healthcare) database. Open an ingredient to browse its citations — links open the study on PubMed or the publisher’s site.

Magnesium 82 references
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  3. Dahle LO, Berg G, Hammar M, et al. The effect of oral magnesium substitution on pregnancy-induced leg cramps. Am J Obstet Gynecol 1995;173:175-80. PubMed
  4. Hansten PD, Horn JR. Drug Interactions Analysis and Management. Vancouver, WA: Applied Therapeutics Inc., 1997 and updates.
  5. Peikert A, Wilimzig C, Kohne-Volland R. Prophylaxis of migraine with oral magnesium: results from a prospective, multi-center, placebo-controlled and double-blind randomized study. Cephalalgia 1996;16:257-63. PubMed
  6. Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride. Washington, DC: National Academy Press, 1999. Available at: http://books.nap.edu/books/0309063507/html/index.html.
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  8. Ryan MP. Diuretics and potassium/magnesium depletion. Directions for treatment. Am J Med 1987;82:38-47.. PubMed
  9. Hollifield JW. Magnesium depletion, diuretics, and arrhythmias. Am J Med 1987;82:30-7.. PubMed
  10. Heidenreich O. Mode of action of conventional and potassium-sparing diuretics--aspects with relevance to Mg-sparing effects. Magnesium 1984;3:248-56..
  11. Pfaffenrath V, Wessely P, Meyer C, et al. Magnesium in the prophylaxis of migraine--a double-blind placebo-controlled study. Cephalalgia 1996;16:436-40.. PubMed
  12. Wang F, Van Den Eeden SK, Ackerson LM, et al. Oral magnesium oxide prophylaxis of frequent migrainous headache in children: a randomized, double-blind, placebo-controlled trial. Headache 2003;43:601-10.. PubMed
  13. Sompolinsky D, Samra Z. Influence of magnesium and manganese on some biological and physical properties of tetracycline. J Bacteriol 1972;110:468-76.. PubMed
  14. Jeyabalan A, Caritis SN. Pharmacologic inhibition of preterm labor. Clin Obstet Gynecol 2002;45:99-113. PubMed
  15. Mittendorf R, Dambrosia J, Pryde PG, et al. Association between the use of antenatal magnesium sulfate in preterm labor and adverse health outcomes in infants. Am J Obstet Gynecol 2002;186:1111-8.. PubMed
  16. Witlin AG, Sibai BM. Magnesium sulfate therapy in preeclampsia and eclampsia. Obstet Gynecol 1998;92:883-9.. DOI
  17. Crowther CA, Hiller JE, Doyle LW. Magnesium sulphate for preventing preterm birth in threatened preterm labour. Cochrane Database Syst Rev 2002;4:CD001060. . PubMed
  18. Davey MJ, Teubner D. A randomized controlled trial of magnesium sulfate, in addition to usual care, for rate control in atrial fibrillation. Ann Emerg Med 2005;45:347-53.. PubMed
  19. L'Hommedieu CS, Nicholas D, Armes DA, et al. Potentiation of magnesium sulfate--induced neuromuscular weakness by gentamicin, tobramycin, and amikacin. J Pediatr 1983;102:629-31..
  20. Dunn CJ, Goa KL. Risedronate: a review of its pharmacological properties and clinical use in resorptive bone disease. Drugs 2001;61:685-712..
  21. Kass L, Weekes J, Carpenter L. Effect of magnesium supplementation on blood pressure: a meta-analysis. Eur J Clin Nutr 2012;66:411-8. PubMed
  22. Koontz SL, Friedman SA, Schwartz ML. Symptomatic hypocalcemia after tocolytic therapy with magnesium sulfate and nifedipine. Am J Obstet Gynecol. 2004;190(6):1773-6. PubMed
  23. Snyder SW, Cardwell MS. Neuromuscular blockade with magnesium sulfate and nifedipine. Am J Obstet Gynecol. 1989;161(1):35-6. PubMed
  24. Waisman GD, Mayorga LM, Cámera MI, et al. Magnesium plus nifedipine: potentiation of hypotensive effect in preeclampsia? Am J Obstet Gynecol. 1988;159(2):308-9. PubMed
  25. Brown DD, Juhl RP. Decreased bioavailability of digoxin due to antacids and kaolin-pectin. N Engl J Med. 1976;295(19):1034-7. PubMed
  26. Allen MD, Greenblatt DJ, Harmatz JS, et al. Effect of magnesium--aluminum hydroxide and kaolin--pectin on absorption of digoxin from tablets and capsules. J Clin Pharmacol. 1981;21(1):26-30. PubMed
  27. Ravn HB, Vissinger H, Kristensen SD, et al. Magnesium inhibits platelet activity--an in vitro study. Thromb Haemost. 1996;76(1):88-93. DOI
  28. Ravn HB, Kristensen SD, Vissinger H, et al. Magnesium inhibits human platelets. Blood Coagul Fibrinolysis. 1996;7(2):241-4. PubMed
  29. Ravn HB, Vissinger H, Kristensen SD, et al. Magnesium inhibits platelet activity--an infusion study in healthy volunteers. Thromb Haemost. 1996;75(6):939-44. DOI
  30. Neuvonen PJ, Kivistö KT. The effects of magnesium hydroxide on the absorption and efficacy of two glibenclamide preparations. Br J Clin Pharmacol. 1991;32(2):215-20. PubMed
  31. Kivistö KT, Neuvonen PJ. Enhancement of absorption and effect of glipizide by magnesium hydroxide. Clin Pharmacol Ther. 1991;49(1):39-43. PubMed
  32. Neuvonen PJ, Kivistö KT. Enhancement of drug absorption by antacids. An unrecognised drug interaction. Clin Pharmacokinet. 1994;27(2):120-8. PubMed
  33. Shechter, M., Merz, C. N., Paul-Labrador, M., Meisel, S. R., Rude, R. K., Molloy, M. D., Dwyer, J. H., Shah, P. K., and Kaul, S. Beneficial antithrombotic effects of the association of pharmacological oral magnesium therapy with aspirin in coronary heart
  34. Ganzevoort, J. W., Hoogerwaard, E. M., and van der Post, J. A. [Hypocalcemic delirium due to magnesium sulphate therapy in a pregnant woman with pre-eclampsia]. Ned.Tijdschr.Geneeskd. 8-3-2002;146(31):1453-1456.
  35. Horner, S. M. Efficacy of intravenous magnesium in acute myocardial infarction in reducing arrhythmias and mortality. Meta-analysis of magnesium in acute myocardial infarction. Circulation 1992;86(3):774-779. PubMed
  36. Azria, E., Tsatsaris, V., Goffinet, F., Kayem, G., Mignon, A., and Cabrol, D. [Magnesium sulfate in obstetrics: current data]. J Gynecol.Obstet.Biol.Reprod.(Paris) 2004;33(6 Pt 1):510-517.
  37. Magee, L. A., Miremadi, S., Li, J., Cheng, C., Ensom, M. H., Carleton, B., Cote, A. M., and von Dadelszen, P. Therapy with both magnesium sulfate and nifedipine does not increase the risk of serious magnesium-related maternal side effects in women with p
  38. Henyan, N. N., Gillespie, E. L., White, C. M., Kluger, J., and Coleman, C. I. Impact of intravenous magnesium on post-cardiothoracic surgery atrial fibrillation and length of hospital stay: a meta-analysis. Ann.Thorac.Surg. 2005;80(6):2402-2406. PubMed
  39. Li, J., Zhang, Q., Zhang, M., and Egger, M. Intravenous magnesium for acute myocardial infarction. Cochrane.Database.Syst.Rev. 2007;(2):CD002755. PubMed
  40. Doyle, L. W., Crowther, C. A., Middleton, P., Marret, S., and Rouse, D. Magnesium sulphate for women at risk of preterm birth for neuroprotection of the fetus. Cochrane.Database.Syst.Rev. 2009;(1):CD004661. PubMed
  41. Han, S., Crowther, C. A., and Moore, V. Magnesium maintenance therapy for preventing preterm birth after threatened preterm labour. Cochrane.Database.Syst.Rev. 2010;(7):CD000940. PubMed
  42. Duley, L., Gulmezoglu, A. M., Henderson-Smart, D. J., and Chou, D. Magnesium sulphate and other anticonvulsants for women with pre-eclampsia. Cochrane.Database.Syst.Rev. 2010;(11):CD000025. PubMed
  43. Conde-Agudelo, A., Romero, R., and Kusanovic, J. P. Nifedipine in the management of preterm labor: a systematic review and metaanalysis. Am J Obstet.Gynecol. 2011;204(2):134-20. PubMed
  44. Wong, G. K., Boet, R., Poon, W. S., Chan, M. T., Gin, T., Ng, S. C., and Zee, B. C. Intravenous magnesium sulphate for aneurysmal subarachnoid hemorrhage: an updated systemic review and meta-analysis. Crit Care 2011;15(1):R52. PubMed
  45. Magee, L., Sawchuck, D., Synnes, A., and von, Dadelszen P. SOGC Clinical Practice Guideline. Magnesium sulphate for fetal neuroprotection. J Obstet.Gynaecol.Can. 2011;33(5):516-529.
  46. Doyle, L. W. Antenatal magnesium sulfate and neuroprotection. Curr Opin Pediatr 2012;24(2):154-159. PubMed
  47. McDonald, S. D., Lutsiv, O., Dzaja, N., and Duley, L. A systematic review of maternal and infant outcomes following magnesium sulfate for pre-eclampsia/eclampsia in real-world use. Int J Gynaecol.Obstet. 2012;118(2):90-96. PubMed
  48. Gordon, M., Naidoo, K., Akobeng, A. K., and Thomas, A. G. Osmotic and stimulant laxatives for the management of childhood constipation. Cochrane.Database.Syst.Rev. 2012;7:CD009118. PubMed
  49. Dodd, J. M., Crowther, C. A., and Middleton, P. Oral betamimetics for maintenance therapy after threatened preterm labour. Cochrane.Database.Syst.Rev. 2012;12:CD003927. PubMed
  50. Wu, X., Wang, C., Zhu, J., Zhang, C., Zhang, Y., and Gao, Y. Meta-analysis of randomized controlled trials on magnesium in addition to beta-blocker for prevention of postoperative atrial arrhythmias after coronary artery bypass grafting. BMC.Cardiovasc.D PubMed
  51. Thorp, J. M., Jr., Katz, V. L., Campbell, D., and Cefalo, R. C. Hypersensitivity to magnesium sulfate. Am.J.Obstet.Gynecol. 1989;161(4):889-890. PubMed
  52. Duley L and Gulmezoglu AM. Magnesium sulphate versus lytic cocktail for eclampsia. Cochrane Database of Systematic Reviews 2000;(3) PubMed
  53. Gibbins KJ, Browning KR, Lopes VV, Anderson BL, Rouse DJ. Evaluation of the clinical use of magnesium sulfate for cerebral palsy prevention. Obstet Gynecol 2013;121(2 Pt 1):235-40. PubMed
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Ceylon Cinnamon 22 references
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Terminalia 9 references
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  9. Eltimamy M, Elshamarka M, Aboelsaad M, Sayed M, Moawad H. Effects of alcoholic extract of Terminalia Chebula dried fruit on blood biochemical profile in diabetic rats. J Diabetes Metab Disord 2022;21(1):159-170. PubMed

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Indian Gooseberry 6 references
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Black Pepper 29 references
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Shilajit 8 references
  1. Sadeghi SMH, Hosseini Khameneh SM, Khodadoost M, et al. Efficacy of momiai in tibia fracture repair: A randomized double-blinded placebo-controlled clinical trial. J Altern Complement Med 2020;26(6):521-528.
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Silicon 19 references
  1. Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington, DC: National Academy Press, 2002.
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  19. Boqué N, Valls RM, Pedret A, Puiggrós F, Arola L, Solà R. Relative absorption of silicon from different formulations of dietary supplements: a pilot randomized, double-blind, crossover post-prandial study. Sci Rep 2021;11(1):16479. PubMed

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DISCLAIMER: Currently this does not check for drug-drug interactions. This is not an all-inclusive comprehensive list of potential interactions and is for informational purposes only. Not all interactions are known or well-reported in the scientific literature, and new interactions are continually being reported. Input is needed from a qualified healthcare provider including a pharmacist before starting any therapy. Application of clinical judgment is necessary.

© 2021 Therapeutic Research Center, LLC

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