Major interaction on record — check this product against your medications before combining. Based on 12 of 13 ingredients. Check your meds →
Dietary supplement

Liver Optima Ingredients & Drug Interactions

by NutraKey

Capsule Category: Other Combinations
Most serious interaction: Major
The interaction bottom line Most serious interaction: Major

Liver Optima is a dietary supplement by NutraKey with 13 active ingredients. Its ingredients are commonly taken for memory and cognitive support, nerve pain (neuropathy), energy and fatigue.Based on those ingredients, 1,658 medications have a known interaction with it, the most serious rated major. The ingredients most likely to interact are Barberry, Turmeric, Milk Thistle Seed Extract. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.

HelloPharmacist Scorecard of Liver Optima by NutraKey

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

What’s inside

Full disclosure
Ingredient Transparency · database check
Full

Every active ingredient lists its own amount on the label.

Why this rating?
  • The label discloses an exact amount for 13 of its 13 active ingredients.
  • No proprietary blends here — you can verify the dose of every single component.

Liver Optima contains 13 active ingredients: L-glutathione, acetyl-L-carnitine, N-acetyl cysteine, turmeric, barberry, schisandra, L-methionine, milk thistle seed extract, grapeseed extract, bupleurum root concentrate, dandelion root concentrate, scute root concentrate, and pueraria (kudzu) root concentrate. These ingredients are included for their traditional liver-supporting roles and various other proposed benefits.

The product also contains inactive ingredients (gelatin and rice flour) as a capsule filler and binder.

Does it work?

Strong evidence
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
Strong

Clinical evidence supports at least one of this product's ingredients for its stated purpose.

Why this rating?
  • The label markets this product for: liver health and detoxification support.
  • We looked for evidence on: Acetaminophen poisoning, Alcohol-related liver disease, Biliary disorders, Chemotherapy-induced hepatotoxicity, hepatic function, cirrhosis — and 2 related terms.
  • The strongest evidence on file: N-acetyl Cysteine (nac) is rated "Effective" for Acetaminophen poisoning (Natural Medicines).
  • Also on file: Turmeric is rated "Possibly Effective" for Nonalcoholic fatty liver disease (NAFLD).
  • Also on file: Methionine is rated "Insufficient Reliable Evidence To Rate" for Acetaminophen poisoning.

The evidence for these ingredients is mixed and often limited. Acetyl-L-carnitine is possibly effective for age-related cognitive decline, Alzheimer disease, alcohol use disorder, diabetic nerve pain (neuropathy), and depression.

N-acetyl cysteine is effective for acetaminophen poisoning and atelectasis (collapsed lung tissue), and possibly effective for bronchitis. Turmeric is possibly effective for depression, high cholesterol (hyperlipidemia), and hay fever.

L-methionine is possibly effective for neural tube birth defects. Milk thistle is possibly effective for type 2 diabetes.

Grapeseed extract is possibly effective for chronic venous insufficiency (poor circulation in the legs) and possibly ineffective for chemotherapy-related nausea, hay fever, and obesity. Kudzu is possibly effective for alcohol use disorder.

For barberry, schisandra, bupleurum, dandelion, and scute, the evidence is insufficient to establish effectiveness for the conditions studied. Overall, while some ingredients have promising data for specific uses, the product as a whole lacks established effectiveness for general liver health.

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 12 of the 12 matched ingredients.
  • Pregnancy & breastfeeding safety ratings cover 12 of 12.
  • General safety write-ups exist for 12 of 12.
  • Remember: this measures how much safety information exists. Thin data is not the same as being safe.

Most ingredients are generally well tolerated at typical doses, but important safety notes exist. Acetyl-L-carnitine is generally well tolerated short-term, but long-term safety is not fully established; it should be avoided during breastfeeding.

Common side effects include agitation, dry mouth, headache, insomnia, reduced appetite, and a fishy odor to urine, breath, and sweat. N-acetyl cysteine is generally well tolerated at typical doses; common side effects are diarrhea, dry mouth, heartburn, nausea, and vomiting.

Turmeric is generally safe as food but concentrated supplements may cause liver problems in rare cases; side effects include constipation, diarrhea, nausea, vomiting, and headache. Barberry should be avoided during pregnancy and breastfeeding due to safety concerns.

Schisandra is generally well tolerated short-term; avoid it during pregnancy and breastfeeding. L-methionine is well tolerated in food amounts; supplement safety during pregnancy and breastfeeding is not proven.

Milk thistle is generally well tolerated but should be avoided during pregnancy; side effects include bloating, diarrhea, nausea, and headache. Grapeseed extract appears safe; grapes as food are fine during pregnancy and breastfeeding, but concentrated supplements are not well studied.

Bupleurum, dandelion, and scute have limited human safety data and should be avoided during pregnancy and breastfeeding. Kudzu is generally well tolerated short-term; avoid during pregnancy and breastfeeding.

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?
  • 11 of the 12 matched ingredients can interact with medications — Milk Thistle, Schisandra, European Barberry, Grape, Bupleurum, 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; lithium.
  • For scale: 1,659 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 Liver Optima, double-check if you use nitroglycerin (Major severity) — this is a serious concern. Next, confirm with your doctor or pharmacist if you take blood pressure medications, blood thinners (anticoagulants and antiplatelets), diabetes drugs, antidepressants or other serotonergic drugs, thyroid hormone replacement, chemotherapy drugs, tacrolimus, midazolam, methotrexate, tamoxifen, or lithium.

This product has documented interactions with all of these drug types across its multiple ingredients.

Check your own medication Run your meds through the checker above

The bottom line

Scorecard at a glanceFully disclosed formula with clinical evidence supporting its stated purpose. Major medication interactions have been identified, and safety information is well characterized.

Liver Optima contains multiple ingredients with interactions affecting a large number of medications, most notably N-acetyl cysteine's serious interaction with nitroglycerin. If you take any blood pressure medications, blood thinners, diabetes drugs, antidepressants, chemotherapy, or numerous other medications, you need to check this product against your specific drugs before starting.

Talk with your doctor or pharmacist about whether this product is right for you.

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

Assessment coverage: 12 of 13 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated Jun 22, 2023.

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 Liver Optima, straight from the product label.

Brand NutraKey
Barcode (UPC) 456355734136
Net contents 90 Capsule(s)
Market status On market
Date entered into DSLD Jun 22, 2023
DSLD ID 287416
Product type Other Combinations
Supplement form Capsule
Dietary claims / uses Nutrient, All Other, Structure/Function
Intended target group(s) Adult (18 - 50 Years)
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 Liver Optima by NutraKey, 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:
3 Capsule(s)
Maximum serving Sizes:
3 Capsule(s)
Servings per container
30
UPC/BARCODE
456355734136
IngredientAmount% DV
L-Glutathione100 mg--
Acetyl-L-Carnitine100 mg--
N-Acetyl Cysteine100 mg--
Turmeric30 mg--
Barberry30 mg--
Schisandra50 mg--
L-Methionine30 mg--
Milk Thistle Seed Extract500 mg--
Grapeseed extract100 mg--
Bupleurum Root Concentrate100 mg--
Dandelion Root Concentrate100 mg--
Scute Root Concentrate50 mg--
Pueraria Root Concentrate50 mg--

Other ingredients: Gelatin, Rice Flour

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.
Formula

Comprehensive liver health and detox formula Liver Optima is a carefully formulated blend of botanical extracts and antioxidants designed to be comprehensive solution for natural liver support and detoxification.

Milk thistle has been shown in numerous clinical studies to support healthy liver function. N-acetyl cysteine (NAC) and L-methionine are two amino acids well known for their ability to enhance glutathione production in the liver. Glutathione is a major antioxidant that plays an essential role in liver detoxification.

Formulation

Each of its ingredients contribute unique properties that fortify the body and help support optimum liver health.

13 active detoxifying ingredients Promote optimal liver health Protects against free-radicals Stabilize metabolism Antioxidants protect your liver Antioxidants protect healthy cells from harmful free radicals and other toxins that build up in your body. Free radicals are molecules are that can cause damage to healthy cells and make them unstable. Neutralizing free radicals is an important part of detoxification.

Health essentials Ultra pure ingredients

Ultra micronized Max bioavailability Rejuvenating botanical formula Support healthy liver function Detoxification and cleansing 13 active detoxification ingredients

Pharmaceutical grade

High-performance liquid chromatography (HPLC) verified

General Statements

Nutrakeyhealth.com Follow us free giveaways Facebook Pinterest Instagram Twitter #MakeLifeBetter

Pure nutrition Go green

Brand IP Statement(s)

NutraKey High Performance Inc

FDA Statement of Identity

Dietary Supplement

Suggested/Recommended/Usage/Directions

Recommended use: Take 1 serving (3 capsules) with water or your favorite beverage in the morning or mid-day before lunch. To maximize results, drink at least 64 ounces of water daily while using this product.

Precautions

Warning: Pregnant or lactating women, diabetics, hypoglycemics, and people with known medical conditions and/or taking drugs should consult with a licensed physician and/or pharmacist prior to taking dietary supplements.

Do not use if seal is broken.

FDA Disclaimer Statement

These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.

Seals/Symbols

Made in the USA

See for yourself

Liver Optima by NutraKey label

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

What’s inside

The Ingredients in Liver Optima by NutraKey

These are the 13 active ingredients this product is made of. Select any to open its full monograph.

Serving size3 Capsule(s) Dosage formCapsule Servings per container30 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.

L-Glutathione

100 mg per serving

Acetyl-L-Carnitine

Interacts with
203 drugs
100 mg per serving

Acetyl-L-carnitine is a form of the amino acid carnitine that the body uses to help produce energy in cells. It is most studied for nerve pain and mem...

Acetyl-L-Carnitine monograph & interactions

N-Acetyl Cysteine

Interacts with
294 drugs
100 mg per serving

N-acetyl cysteine (NAC) is a supplement form of the amino acid cysteine and a building block for the antioxidant glutathione. It has well-established...

N-Acetyl Cysteine monograph & interactions

Turmeric

Interacts with
1,133 drugs
30 mg per serving

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

Turmeric monograph & interactions

Barberry

Interacts with
1,210 drugs
30 mg per serving

European barberry is a shrub whose root, bark, and berries contain berberine, a bitter plant alkaloid that has been studied mostly in isolated form. S...

Barberry monograph & interactions

Schisandra

Interacts with
803 drugs
50 mg per serving

Schisandra is a traditional Chinese medicine berry used as an adaptogen for stress, fatigue, and liver support. Human evidence is limited and most cla...

Schisandra monograph & interactions

L-Methionine

No known
interactions
30 mg per serving

Methionine is an essential amino acid that your body needs for protein building and many basic chemical reactions. Most people get enough from a norma...

L-Methionine monograph & interactions

Milk Thistle Seed Extract

Interacts with
954 drugs
500 mg per serving Form: Silymarin

Milk thistle is a popular herbal supplement most often used for liver health, and its main active component is a group of compounds called silymarin....

Milk Thistle Seed Extract monograph & interactions

Grapeseed extract

Interacts with
910 drugs
100 mg per serving Form: Polyphenols

Grapes and grape products like grape seed extract contain antioxidant compounds such as resveratrol and proanthocyanidins that may support heart and b...

Grapeseed extract monograph & interactions

Bupleurum Root Concentrate

Interacts with
327 drugs
100 mg per serving

Bupleurum (Chai Hu) is a root used in traditional Chinese medicine, usually as part of multi-herb formulas, for liver, digestive, and fever-related co...

Bupleurum Root Concentrate monograph & interactions

Dandelion Root Concentrate

Interacts with
457 drugs
100 mg per serving

Dandelion is a common plant used in food and traditional medicine, often promoted as a natural 'water pill' and digestive aid. Human evidence for thes...

Dandelion Root Concentrate monograph & interactions

Scute Root Concentrate

Interacts with
946 drugs
50 mg per serving

Baikal skullcap is a traditional Chinese herb (Huang Qin) used for inflammation, allergies, and infections, with active compounds like baicalin and ba...

Scute Root Concentrate monograph & interactions

Pueraria Root Concentrate

Interacts with
584 drugs
50 mg per serving Form: Pueraria thomsonii

Kudzu is a fast-growing vine whose root has long been used in traditional Chinese medicine and is now studied mostly for reducing alcohol intake. Earl...

Pueraria Root Concentrate monograph & interactions

Other (inactive) ingredients: Gelatin, Rice Flour. These complete the product’s ingredient list but are not active constituents.

Interaction report

Liver Optima by NutraKey Drug Interactions

Want to check YOUR meds against Liver Optima?

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
1,658Drugs
1 Major 1,657 Moderate

Ingredients driving the most interactions

Barberry 1,210
Turmeric 1,133

Each ingredient & the kinds of drugs it affects

For each ingredient in Liver Optima 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.

Barberry8 drug types · 1,210 drugs

Anticholinergic Drugs

Theoretically, taking European barberry with anticholinergic drugs might cause additive effects.
In vitro evidence suggests that European barberry might have anticholinergic properties.

Likelihood Possible Evidence D
Anticoagulant/Antiplatelet Drugs

Theoretically, European barberry may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
In vitro and animal evidence suggest that berberine, a constituent of European barberry, might inhibit platelet aggregation. Theoretically, European barberry might have a similar effect.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, taking European barberry with antidiabetes drugs might increase the risk of hypoglycemia.
Preliminary clinical evidence suggests that European barberry juice reduces fasting glucose levels in patients with type 2 diabetes who are also taking antidiabetes drugs. Additionally, some animal studies show that berberine, a constituent of European barberry, has antiglycemic potential. Monitor blood glucose levels closely.

Likelihood Possible Evidence B
Antihypertensive Drugs

Theoretically, taking European barberry with antihypertensive drugs might increase the risk of hypotension.
Animal and human research suggests that European barberry extracts can have hypotensive effects.

Likelihood Possible Evidence D
Cholinergic Drugs

Theoretically, taking European barberry with cholinergic drugs might decrease the effects of cholinergic drugs.
In vitro evidence suggests that European barberry might have anticholinergic properties.

Likelihood Possible Evidence D
Cns Depressants

Theoretically, concomitant use with drugs that have sedative properties may cause additive effects.
Animal research suggests that berberine, a constituent of European barberry, might have sedative effects. Theoretically, European barberry might have a similar effect.

Likelihood Possible Evidence D
Cyclosporine (Neoral, Sandimmune)

Theoretically, concomitant use with cyclosporine may cause additive effects.
Berberine, a constituent of European barberry, can reduce the metabolism and increase serum levels of cyclosporine. This effect is attributed to the ability of berberine to inhibit cytochrome P450 3A4 (CYP3A4), which metabolizes cyclosporine. Theoretically, European barberry might have a similar effect.

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

Theoretically, European barberry might increase the levels and clinical effects of CYP3A4 substrates.
There is very preliminary evidence suggesting that berberine, a constituent of European barberry, might inhibit the CYP3A4 enzyme. Theoretically, European barberry might have a similar effect.

Likelihood Possible Evidence D

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

Milk Thistle Seed Extract17 drug types · 954 drugs

Antidiabetes Drugs

Taking milk thistle with antidiabetes drugs may increase the risk of hypoglycemia.
Clinical research shows that milk thistle extract, alone or along with tree turmeric extract, can lower blood glucose levels and glycated hemoglobin (HbA1c) in patients with type 2 diabetes, including those already taking antidiabetes drugs. Additionally, animal research shows that milk thistle extract increases the metformin maximum plasma concentration and area under the curve and decreases the renal clearance of metformin, due to inhibition of the multi-drug and toxin extrusion protein 1 (MATE1) renal tubular transport protein.

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

Theoretically, milk thistle might inhibit CYP2B6.
An in vitro study shows that silybin, a constituent of milk thistle, binds to and noncompetitively inhibits CYP2B6. Additionally, silybin might downregulate the expression of CYP2B6 by decreasing mRNA and protein levels.

Likelihood Possible Evidence D
Glucuronidated Drugs

Theoretically, milk thistle might affect the clearance of drugs that undergo glucuronidation.
Laboratory research shows that milk thistle constituents inhibit uridine diphosphoglucuronosyl transferase (UGT), the major phase 2 enzyme that is responsible for glucuronidation. Theoretically, this could decrease the clearance and increase levels of glucuronidated drugs. Other laboratory research suggests that a milk thistle extract of silymarin might inhibit beta-glucuronidase, although the significance of this effect is unclear.

Likelihood Possible Evidence D
Ledipasvir

Theoretically, milk thistle might increase the levels and clinical effects of ledipasvir.
Animal research in rats shows that milk thistle increases the area under the curve (AUC) for ledipasvir and slows its elimination.

Likelihood Possible Evidence D
Morphine

Theoretically, concomitant use of milk thistle with morphine might affect serum levels of morphine and either increase or decrease its effects.
Animal research shows that milk thistle reduces serum levels of morphine by up to 66%. In contrast, laboratory research shows that milk thistle constituents inhibit uridine diphosphoglucuronosyl transferase (UGT), the major phase 2 enzyme that is responsible for glucuronidation. Theoretically, this could decrease the clearance and increase morphine levels. The effect of taking milk thistle on morphine metabolism in humans is not known.

Likelihood Possible Evidence D
Raloxifene (Evista)

Theoretically, milk thistle might decrease the clearance and increase levels of raloxifene.
Laboratory research suggests that the milk thistle constituents silibinin and silymarin inhibit the glucuronidation of raloxifene in the intestines.

Likelihood Possible Evidence D
Sirolimus (Rapamune)

Milk thistle might decrease the clearance of sirolimus.
Pharmacokinetic research shows that a milk thistle extract of silymarin decreases the apparent clearance of sirolimus in hepatically impaired renal transplant patients. It is unclear if this interaction occurs in patients without hepatic impairment.

Likelihood Possible Evidence B
Sofosbuvir (Solvaldi)

Theoretically, milk thistle might decrease the levels and clinical effects of sofosbuvir.
Animal research in rats shows that milk thistle reduces the metabolism of sofosbuvir, as well as the hepatic uptake of its active metabolite.

Likelihood Possible Evidence D
Tamoxifen (Nolvadex)

Theoretically, the milk thistle constituent silibinin might increase tamoxifen levels and interfere with its conversion to an active metabolite.
Animal research suggests that the milk thistle constituent silibinin might increase plasma levels of tamoxifen and alter its conversion to an active metabolite. The mechanism appears to involve inhibition of pre-systemic metabolism of tamoxifen by cytochrome P450 (CYP) 2C9 and CYP3A4, and inhibition of P-glycoprotein-mediated efflux of tamoxifen into the intestine for excretion. Whether this interaction occurs in humans is not known.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Theoretically, milk thistle might increase the effects of warfarin.
In one case report, a man stabilized on warfarin experienced an increase in INR from 2.64 to 4.12 after taking a combination product containing milk thistle 200 mg daily, as well as dandelion, wild yam, niacinamide, and vitamin B12. Levels returned to normal after stopping the supplement. Although a direct correlation between milk thistle and the change in INR cannot be confirmed, some in vitro research suggests that milk thistle might inhibit cytochrome P450 2C9 (CYP2C9), an enzyme involved in the metabolism of various drugs, including warfarin.

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

It is unclear if milk thistle inhibits CYP2C9; research is conflicting.
In vitro research suggests that milk thistle might inhibit CYP2C9. Additionally, 3 case reports from the World Health Organization (WHO) adverse drug reaction database describe increased toxicity in patients taking milk thistle and cancer medications that are CYP2C9 substrates, including imatinib and capecitabine. However, contradictory clinical research shows that milk thistle extract does not inhibit CYP2C9 or significantly affect levels of the CYP2C9 substrate tolbutamide. Differences in results could be due to differences in dosages or formulations utilized.

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

It is unclear if milk thistle inhibits CYP3A4; research is conflicting.
While laboratory research shows conflicting results, pharmacokinetic research shows that taking milk thistle extract 420-1350 mg daily does not significantly affect the metabolism of the CYP3A4 substrates irinotecan, midazolam, or indinavir. However, 8 case reports from the World Health Organization (WHO) adverse drug reaction database describe increased toxicity in patients taking milk thistle and cancer medications that are CYP3A4 substrates, including gefitinib, sorafenib, doxorubicin, and vincristine.

Likelihood Unlikely Evidence D
Estrogens

Theoretically, milk thistle might interfere with estrogen therapy through competition for estrogen receptors.
Animal research suggests that a milk thistle extract of silymarin binds to estrogen receptor beta.

Likelihood Possible Evidence D
Hmg-Coa Reductase Inhibitors ("Statins")

Theoretically, milk thistle might interfere with statin therapy by decreasing the activity of organic anion transporting polypeptide 1B1 (OATB1B1) and inhibiting breast cancer resistance protein (BCRP).
Preliminary evidence suggests that a milk thistle extract of silymarin can decrease the activity of the OATP1B1, which transports HMG-CoA reductase inhibitors into the liver to their site of action, and animal research shows this increases the maximum plasma concentration of pitavastatin and pravastatin. The silibinin component also inhibits BCRP, which transports statins from the liver into the bile for excretion. However, in a preliminary study in healthy males, silymarin 140 mg three times daily had no effect on the pharmacokinetics of a single 10 mg dose of rosuvastatin.

Likelihood Unlikely Evidence D
Indinavir (Crixivan)

Theoretically, milk thistle may induce cytochrome P450 3A4 (CYP3A4) enzymes and increase the metabolism of indinavir; however, results are conflicting.
One pharmacokinetic study shows that taking milk thistle (Standardized Milk Thistle, General Nutrition Corp.) 175 mg three times daily in combination with multiple doses of indinavir 800 mg every 8 hours decreases the mean trough levels of indinavir by 25%. However, results from the same pharmacokinetic study show that milk thistle does not affect the overall exposure to indinavir. Furthermore, two other pharmacokinetic studies show that taking specific milk thistle extract (Legalon, Rottapharm Madaus; Thisilyn, Nature's Way) 160-450 mg every 8 hours in combination with multiple doses of indinavir 800 mg every 8 hours does not reduce levels of indinavir.

Likelihood Unlikely Evidence B
Organic Anion-Transporting Polypeptide Substrates (Oatp)

Milk thistle may inhibit one form of OATP, OATP-B1, which could reduce the bioavailability and clinical effects of OATP-B1 substrates.
In vitro research shows that milk thistle inhibits OATP-B1. Two case reports from the World Health Organization (WHO) adverse drug reaction database describe increased toxicity in patients taking milk thistle and cancer medications that are OATP substrates, including sorafenib and methotrexate. OATPs are expressed in the small intestine and liver and are responsible for the uptake of drugs and other compounds into the body. Inhibition of OATP may reduce the bioavailability of oral drugs that are substrates of OATP.

Likelihood Possible Evidence D
P-Glycoprotein Substrates

Theoretically, milk thistle might increase the absorption of P-glycoprotein substrates. However, this effect does not seem to be clinically significant.
In vitro research shows that milk thistle can inhibit P-glycoprotein activity and 1 case report from the World Health Organization (WHO) adverse drug reaction database describes increased abdominal pain in a patient taking milk thistle and the cancer medication vincristine, a P-glycoprotein substrate, though this patient was also taking methotrexate. However, a small pharmacokinetic study in healthy volunteers shows that taking milk thistle (Enzymatic Therapy Inc.) 900 mg, standardized to 80% silymarin, in 3 divided doses daily for 14 days does not affect absorption of digoxin, a P-glycoprotein substrate.

Likelihood Unlikely Evidence B

Scute Root Concentrate12 drug types · 946 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, Baikal skullcap might increase the risk of bleeding when used concomitantly with anticoagulant and antiplatelet drugs.
Preliminary clinical research suggests that taking capsules containing a combination of astragalus, goldthread, and Baikal skullcap daily for 4 weeks inhibits platelet aggregation; the effect seems to be similar to that of aspirin 50 mg daily. It is unclear if this effect is due to Baikal skullcap, other ingredients, or the combination.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, concomitant use of Baikal skullcap with antidiabetes drugs might enhance blood glucose lowering effects.
Baicalein, a constituent of Baikal skullcap, has alpha-glucosidase inhibitory activity in vitro. Animal research also suggests that Baikal skullcap enhances the antidiabetic effects of metformin. However, in a small human study, taking Baikal skullcap extract did not enhance the antidiabetic effects of metformin, although it did modestly lower glucose levels during an oral glucose tolerance test (OGTT). Until more is known, use cautiously.

Likelihood Possible Evidence B
Antihypertensive Drugs

Theoretically, concomitant use of Baikal skullcap with antihypertensive drugs might have additive effects and increase the risk of hypotension.
Animal research suggests that baicalein, a constituent of Baikal skullcap, might lower blood pressure.

Likelihood Possible Evidence D
Antithyroid Drugs

Theoretically, concomitant use of Baikal skullcap and antithyroid drugs may result in additive activity and increase the risk of hypothyroidism.
In an animal hyperthyroid model, Baikal skullcap improved levels of triiodothyronine (T3), thyroxine (T4), and thyroid stimulating hormone (TSH). The clinical significance of this effect is unclear.

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

Theoretically, Baikal skullcap may increase levels of drugs metabolized by CYP1A2 enzymes.
In vitro evidence suggests that constituents of Baikal skullcap inhibit the activity of CYP1A2. This effect has not been reported in humans.

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

Theoretically, Baikal skullcap might increase levels of drugs metabolized by CYP2C19 enzymes.
In vitro evidence suggest that wogonin, a constituent of Baikal skullcap, modestly inhibits the activity of CYP2C19 enzymes. This effect has not been reported in humans.

Likelihood Possible Evidence D
Estrogens

Theoretically, concomitant use of large amounts of Baikal skullcap might interfere with hormone replacement therapy, due to competition for estrogen receptors.
In vitro evidence suggests that Baikal skullcap has estrogenic activity.

Likelihood Possible Evidence D
Lithium

Theoretically, Baikal skullcap might reduce lithium excretion and increase serum levels of lithium.
Baikal skullcap is thought to have diuretic properties, which may reduce lithium excretion. The dose of lithium might need to be decreased.

Likelihood Possible Evidence D
Alcohol (Ethanol)

Theoretically, Baikal skullcap might potentiate the sedative effects of alcohol.
In vitro and animal research suggests that Baikal skullcap binds to GABA-A receptors and causes sedation. Theoretically, Baikal skullcap might potentiate the sedative effects of alcohol. Preliminary clinical research has not identified clinically relevant sedation after use of Baikal skullcap; however, a thorough evaluation of safety outcomes has not been conducted.

Likelihood Unlikely Evidence D
Cns Depressants

Theoretically, Baikal skullcap might cause additive therapeutic and adverse effects when used concomitantly with drugs with sedative properties.
In vitro and animal research suggests that Baikal skullcap binds to GABA-A receptors and causes sedation. Theoretically, Baikal skullcap might cause additive therapeutic and adverse effects when used concomitantly with drugs with sedative properties. Preliminary clinical research has not identified clinically relevant sedation after use of Baikal skullcap; however, a thorough evaluation of safety outcomes has not been conducted.

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

Theoretically, Baikal skullcap might alter the levels and clinical effects of OATP substrates.
Some pharmacokinetic research shows that baicalin, a constituent of Baikal skullcap, can decrease plasma levels of rosuvastatin. The mechanism is thought to involve stimulation of the activity of the organic anion-transporting polypeptide 1B1 (OATP1B1), which transports rosuvastatin into the liver. This decreases plasma levels of the drug, but increases levels at the site of action in the liver. The degree to which rosuvastatin levels are affected depends on the OATP1B1 haplotype of the individual. Baikal skullcap might also affect other OATP1B1 substrates.

Likelihood Possible Evidence B
P-Glycoprotein Substrates

Theoretically, Baikal skullcap might increase levels of drugs transported by P-glycoprotein.
In vitro and animal research suggests that baicalein, oroxylin A, and wogonin, constituents of Baikal skullcap, can inhibit P-glycoprotein. This effect has not been reported in humans.

Likelihood Possible Evidence D

Grapeseed extract9 drug types · 910 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, grape extracts may have antiplatelet effects and may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
In vitro evidence suggests that grape extracts might decrease platelet aggregation.

Likelihood Possible Evidence D
Cyclosporine (Neoral, Sandimmune)

Ingesting grape juice with cyclosporine can reduce cyclosporine absorption.
A small pharmacokinetic study in healthy young adults shows that intake of purple grape juice 200 mL along with cyclosporine can decrease the absorption of cyclosporine by up to 30% when compared with water. Separate doses of grape juice and cyclosporine by at least 2 hours to avoid this interaction.

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

Theoretically, grape juice might reduce the levels of CYP1A2 substrates.
A small pharmacokinetic study in healthy adults shows that ingestion of 200 mL of grape juice decreases phenacetin plasma levels. This is thought to be due to induction of CYP1A2.

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

Theoretically, grape seed extract may increase the levels of CYP2D6 substrates.
In vitro evidence suggests that grape seed extract might inhibit CYP2D6 enzymes. However, this interaction has not been reported in humans.

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

Theoretically, grape seed extract might increase the levels of CYP2E1 substrates.
In vitro and animal research suggests that grape seed proanthocyanidin extract inhibits CYP2E1 enzymes. However, this interaction has not been reported in humans.

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

It is unclear if grape seed extract inhibits or induces CYP3A4; research is conflicting.
In vitro evidence suggests that grape seed extract might inhibit CYP3A4 enzymes. However, evidence from animal research shows that grape seed extract may induce CYP3A4 in the liver. So far, these interactions have not been reported in humans.

Likelihood Possible Evidence D
Midazolam (Versed)

Theoretically, long-term intake of grape seed extract might decrease the effects of midazolam.
Animal research shows that subchronic ingestions of grape seed extract can increase the elimination of intravenous midazolam by increasing hepatic CYP3A4 activity. Single doses of grape seed extract do not appear to affect midazolam elimination.

Likelihood Possible Evidence D
Phenacetin

Grape juice might decrease phenacetin absorption.
A small pharmacokinetic study in healthy adults shows that ingestion of 200 mL of grape juice decreases phenacetin plasma levels. This is thought to be due to induction of cytochrome P450 1A2 (CYP1A2).

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

It is unclear if grape juice or grape seed extract inhibits CYP2C9; research is conflicting.
In vitro evidence shows that grape seed extract or grape juice might inhibit CYP2C9 enzymes. However, a small pharmacokinetic study in healthy adults shows that drinking 8 ounces of grape juice once does not affect the clearance of flurbiprofen, a probe-drug for CYP2C9 metabolism. The effects of continued grape juice consumption are unclear.

Likelihood Unlikely Evidence D

Schisandra12 drug types · 803 drugs

Cyclophosphamide

Theoretically, schisandra might increase the levels and clinical effects of cyclophosphamide.
In vitro research shows that schisandra increases the concentration of cyclophosphamide, likely through inhibition of cytochrome P450 3A4. After multiple doses of the schisandra constituents schisandrin A and schisantherin A, the maximum concentration of cyclophosphamide was increased by 7% and 75%, respectively, while the overall exposure to cyclophosphamide was increased by 29% and 301%, respectively.

Likelihood Probable Evidence D
Cyclosporine (Neoral, Sandimmune)

Schisandra can increase the levels and clinical effects of cyclosporine.
A small observational study in children with aplastic anemia found that taking schisandra with cyclosporine increased cyclosporine trough levels by 93% without increasing the risk of adverse events. However, the dose of cyclosporine was reduced in 9% of children to maintain appropriate cyclosporine blood concentrations.

Likelihood Probable Evidence B
Cytochrome P450 2C19 (Cyp2C19) Substrates

Theoretically, schisandra might increase the levels and clinical effects of CYP2C19 substrates.
In vitro research shows that schisandra inhibits CYP2C19, and animal research shows that schisandra increases the concentration of voriconazole, a CYP2C19 substrate. Theoretically, schisandra may also inhibit the metabolism of other CYP2C19 substrates. This effect has not been reported in humans.

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

Theoretically, schisandra might decrease the levels and clinical effects of CYP2C9 substrates.
In vitro and animal research suggests that schisandra induces CYP2C9 enzymes. This effect has not been reported in humans.

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

Schisandra can increase the levels and clinical effects of drugs metabolized by CYP3A4.
Most clinical and laboratory research shows that schisandra, administered either as a single dose or up to twice daily for 14 days, inhibits CYP3A4 and increases the concentration of CYP3A4 substrates such as cyclophosphamide, midazolam, tacrolimus, and talinolol. Although one in vitro and animal study shows that schisandra may induce CYP3A4 metabolism, this effect appears to be overpowered by schisandra's CYP3A4 inhibitory activity and has not been reported in humans.

Likelihood Probable Evidence D
Midazolam (Versed)

Schisandra can increase the levels and clinical effects of midazolam.
A small pharmacokinetic study in healthy adults shows that taking schisandra extract (Hezheng Pharmaceutical Co.) containing deoxyschizandrin 33.75 mg twice daily for 8 days and a single dose of midazolam 15 mg on day 8 increases the overall exposure to midazolam by about 119%, increases the peak plasma level of midazolam by 86%, and decreases midazolam clearance by about 52%. This effect has been attributed to inhibition of CYP3A4 by schisandra.

Likelihood Probable Evidence B
P-Glycoprotein Substrates

Schisandra might increase the levels and clinical effects of P-glycoprotein substrates.
In vitro research shows that schisandra extracts and constituents such as schisandrin B inhibit P-glycoprotein mediated efflux in intestinal cells and in P-glycoprotein over-expressing cell lines. Additionally, a small clinical study shows that schisandra increases the peak concentration and overall exposure to talinolol, a P-glycoprotein probe substrate. Theoretically, schisandra might inhibit the efflux of other P-glycoprotein substrates.

Likelihood Possible Evidence D
Sirolimus (Rapamune)

Schisandra can increase the levels and clinical effects of sirolimus.
A small pharmacokinetic study in healthy volunteers shows that taking 3 capsules of schisandra (Hezheng Pharmaceutical Company) containing a total of 33.75 mg deoxyschizandrin twice daily for 13 days and then taking a single dose of sirolimus 2 mg increases the overall exposure and peak level of sirolimus by two-fold. This effect is thought to be due to inhibition of cytochrome P450 3A4 by schisandra, as well as possible inhibition of the P-glycoprotein drug transporter.

Likelihood Probable Evidence B
Tacrolimus (Prograf)

Schisandra can increase the levels and clinical effects of tacrolimus.
Clinical research in healthy children and adults, transplant patients, and patients with nephrotic syndrome and various rheumatic immunologic disorders shows that taking schisandra with tacrolimus increases tacrolimus peak levels by 183% to 268%, prolongs or delays time to peak tacrolimus concentrations, increases overall exposure to tacrolimus by 126% to 343%, and decreases tacrolimus clearance by 19% to 73%. This effect is thought to be due to inhibition of P-glycoprotein drug transporter and CYP3A4 and CYP3A5 by schisandra. Some clinical and observational studies suggest that schisandra increases tacrolimus levels similarly in both expressors and non-expressors of CYP3A5, while other studies suggest it does so to a greater degree in CYP3A5 expressors than non-expressors. Animal research suggests that the greatest increase in tacrolimus levels occurs when schisandra is taken either concomitantly or up to 2 hours before tacrolimus, and clinical and observational research in humans suggests that schisandra may increase whole blood levels of tacrolimus and decrease clearance of tacrolimus in a dose-dependent manner.

Likelihood Probable Evidence B
Talinolol

Schisandra can increase the levels and clinical effects of talinolol.
A small pharmacokinetic study in healthy volunteers shows that taking schisandra extract 300 mg twice daily for 14 days with a single dose of talinolol 100 mg on day 14 increases the peak talinolol level by 51% and the overall exposure to talinolol by 47%. This effect is thought to be due to the possible inhibition of cytochrome P450 3A4 and P-glycoprotein by schisandra. tly.

Likelihood Probable Evidence B
Voriconazole (Vfend)

Theoretically, schisandra might increase the levels and clinical effects of voriconazole.
Animal research shows that oral schisandra given daily for 1 or 14 days increases levels of intravenously administered voriconazole, a cytochrome P450 (CYP) 2C19 substrate. This effect is thought to be due to inhibition of CYP2C19 by schisandra. However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Theoretically, schisandra might decrease the levels and clinical effects of warfarin.
Animal research suggests that oral schisandra extract, given daily for 6 days, reduces levels of intravenously administered warfarin. This effect might be due to the induction of cytochrome P450 (CYP) 2C9 metabolism by schisandra. However, this interaction has not been reported in humans.

Likelihood Possible Evidence D

Pueraria Root Concentrate7 drug types · 584 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, kudzu may increase the risk of bleeding if used with antiplatelet or anticoagulant drugs.
Kudzu isoflavones are reported to have antiplatelet activity.

Likelihood Possible Evidence D
Caffeine

Theoretically, taking kudzu with caffeine might increase levels of caffeine.
In healthy males injected with the kudzu constituent puerarin, caffeine clearance and metabolism is inhibited. This effect has been attributed to inhibition of cytochrome P450 1A2 (CYP1A2) enzyme, which is involved in caffeine metabolism. It is unclear if taking kudzu orally would have this same effect.

Likelihood Probable Evidence D
Estrogens

Theoretically, kudzu might alter the effects of estrogen therapy.
Some research suggests that kudzu has estrogenic effects. This may enhance or inhibit the effects of estrogen therapy.

Likelihood Possible Evidence B
Hepatotoxic Drugs

Theoretically, concomitant use might have additive hepatotoxic effects.
There is some concern that kudzu can adversely affect the liver.

Likelihood Possible Evidence D
Methotrexate (Trexall, Others)

Theoretically, taking kudzu with methotrexate might increase the risk of methotrexate toxicity.
Preclinical research suggests that kudzu extract greatly reduces the elimination and increases the toxicity of methotrexate. Kudzu might inhibit organic anion transporters (OATs) that are responsible for hepatobiliary and renal excretion of anions, similar to the interaction between methotrexate and non-steroidal anti-inflammatory drugs (NSAIDs).

Likelihood Possible Evidence D
Tamoxifen (Nolvadex)

Theoretically, kudzu might interfere with tamoxifen activity.
Some research suggests that kudzu may have estrogenic effects.

Likelihood Possible Evidence B
Antidiabetes Drugs

Theoretically, taking kudzu with antidiabetes drugs might increase the risk of hypoglycemia.
Kudzu might lower blood glucose levels and have additive effects in patients treated with antidiabetic agents. The dose of diabetes medications might need to be adjusted.

Likelihood Unlikely Evidence D

Dandelion Root Concentrate7 drug types · 457 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, taking dandelion root along with anticoagulant or antiplatelet drugs might increase the risk of bruising and bleeding.
In vitro research suggests that dandelion root inhibits platelet aggregation.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, dandelion might increase the risk for hypoglycemia when used with antidiabetes drugs.
Laboratory research suggests that dandelion extract may have moderate alpha-glucosidase inhibitor activity and might also increase insulin secretion. Also, in a case report, a 58-year-old woman with type 2 diabetes who was being treated with insulin developed hypoglycemia 2 weeks after beginning to eat salads containing dandelion.

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

Theoretically, dandelion might increase levels of drugs metabolized by CYP1A2.
Laboratory research suggests that dandelion might inhibit CYP1A2. So far, this interaction has not been reported in humans. However, until more is known, watch for an increase in the levels of drugs metabolized by CYP1A2 in patients taking dandelion.

Likelihood Possible Evidence D
Glucuronidated Drugs

Theoretically, dandelion might increase the clearance of drugs that are UDP-glucuronosyltransferase substrates.
There is some preliminary evidence that dandelion might induce UDP-glucuronosyltransferase, a phase II enzyme.

Likelihood Possible Evidence D
Lithium

Theoretically, through diuretic effects, dandelion might reduce excretion and increase levels of lithium.
Animal research suggests that dandelion has diuretic properties. As diuretics can increase serum lithium levels, the dose of lithium might need to be decreased when taken with dandelion.

Likelihood Probable Evidence D
Potassium-Sparing Diuretics

Theoretically, dandelion might increase the risk of hyperkalemia when taken with potassium-sparing diuretics.
Dandelion contains significant amounts of potassium.

Likelihood Possible Evidence D
Quinolone Antibiotics

Theoretically, dandelion might lower fluoroquinolone levels.
Animal research shows that dandelion reduces absorption of ciprofloxacin and can lower levels by 73%. However, this effect has not been reported in humans.

Likelihood Possible Evidence D

Bupleurum Root Concentrate3 drug types · 327 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, bupleurum might increase the risk of bleeding when taken with anticoagulant or antiplatelet drugs.
In vitro research suggests that saikosaponins, constituents of bupleurum, can inhibit platelet aggregation.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, bupleurum might decrease the effects of antidiabetes drugs.
Animal research suggests that saikosaponins, constituents of bupleurum, can increase blood glucose.

Likelihood Possible Evidence D
Immunosuppressants

Theoretically, bupleurum might decrease the effects of immunosuppressants.
In vitro and animal research suggests that bupleurum might stimulate immune function.

Likelihood Possible Evidence D

N-Acetyl Cysteine5 drug types · 294 drugs

Nitroglycerin

N-acetyl cysteine can increase the risk for hypotension and headaches when taken with intravenous or transdermal nitroglycerin.
Clinical research shows that concomitant administration of N-acetyl cysteine and intravenous or transdermal nitroglycerin can cause severe hypotension and intolerable headaches. Furthermore, in vitro research suggests that N-acetyl cysteine increases the anticoagulant activity of nitroglycerin.

Likelihood Probable Evidence B
Activated Charcoal

N-acetyl cysteine might reduce the effects of activated charcoal, while activated charcoal might reduce the absorption of N-acetyl cysteine.
N-acetyl cysteine appears to reduce the capacity of activated charcoal to adsorb acetaminophen and salicylic acid. Conversely, although clinical research suggests that although activated charcoal can reduce the absorption of N-acetyl cysteine by up to 40%, it does not seem to reduce its clinical effects. Other clinical evidence suggests that activated charcoal does not affect the absorption of N-acetyl cysteine.

Likelihood Possible Evidence D
Anticoagulant/Antiplatelet Drugs

Theoretically, N-acetyl cysteine might increase the risk of bleeding when taken with anticoagulant or antiplatelet drugs.
Clinical research suggests that intravenous N-acetyl cysteine decreases prothrombin time, prolongs coagulation time, decreases platelet aggregation, and increases blood loss in surgical patients. Furthermore, in vitro research suggests that N-acetyl cysteine increases the anticoagulant activity of nitroglycerin.

Likelihood Possible Evidence D
Antihypertensive Drugs

Theoretically, N-acetyl cysteine might increase the risk of hypotension when taken with antihypertensive drugs.
Animal research suggests that N-acetyl cysteine potentiates the hypotensive effects of the angiotensin-converting enzyme inhibitors (ACEIs) captopril and enalaprilat. Theoretically, combining N-acetyl cysteine with other antihypertensive drugs might increase the risk of hypotension.

Likelihood Possible Evidence D
Chloroquine (Aralen)

Theoretically, N-acetyl cysteine might interfere with the antimalarial effects of chloroquine.
Animal research suggests that N-acetyl cysteine might reduce the antimalarial effects of chloroquine by increasing cellular levels of glutathione.

Likelihood Possible Evidence D

Acetyl-L-Carnitine4 drug types · 203 drugs

Acenocoumarol (Sintrom)

Theoretically, acetyl-L-carnitine might increase the anticoagulant effects of acenocoumarol.
L-carnitine, the parent compound of acetyl-L-carnitine, might enhance the anticoagulant effects of acenocoumarol, an oral anticoagulant that is similar to warfarin, but shorter-acting. There are at least two case reports of INR elevation when L-carnitine was taken with acenocoumarol. In one case, a 33-year-old male with a previously stable INR had an elevated INR of 4.65 after L-carnitine was started and continued for 10 weeks. INR normalized after discontinuation of the L-carnitine-containing product. It is unclear if such an interaction would also occur with acetyl-L-carnitine.

Likelihood Possible Evidence D
Serotonergic Drugs

Theoretically, acetyl-L-carnitine might increase the risk of serotonergic side effects, including serotonin syndrome and cerebral vasoconstrictive disorders, when taken with serotonergic drugs.
Animal research shows that acetyl-L-carnitine can increase levels of serotonin in the brain.

Likelihood Possible Evidence D
Thyroid Hormone

Theoretically, acetyl-L-carnitine might decrease the effectiveness of thyroid hormone replacement.
L-carnitine appears to act as a peripheral thyroid hormone antagonist by inhibiting entry of thyroid hormone into the nucleus of cells. Taking L-carnitine also seems to diminish some of the symptoms of hyperthyroidism. It is unclear if such an interaction would occur with acetyl-L-carnitine.

Likelihood Probable Evidence B
Warfarin (Coumadin)

Theoretically, acetyl-L-carnitine might increase the anticoagulant effects of warfarin.
L-carnitine, the parent compound of acetyl-L-carnitine, might increase the anticoagulant effects of acenocoumarol, a shorter-acting oral anticoagulant similar to warfarin. There is not enough information to know whether this interaction occurs with acetyl-L-carnitine and warfarin.

Likelihood Possible Evidence D
The maker

Brand information

Manufacturer and brand details for Liver Optima, from the product label.

NutraKey

See all NutraKey products
Name
Nutrakey
Street Address
975 Bennett Drive
City
Longwood
State
FL
ZipCode
32750
Web Address
Nutrakeyhealth.com
Pharmacist Counseling Corner

Liver Optima by NutraKey: Common Questions

Does Liver Optima by NutraKey interact with any medications?
Yes. Based on its ingredients, Liver Optima has a known interaction with 1,658 medications, including 1 rated major. Use the checker to see how it interacts with a specific drug.
How can one product interact with so many drugs?
Liver Optima contains 13 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.
Does this product actually help the liver?
The evidence for these ingredients in general liver health is not established in the data we hold. Some ingredients like milk thistle and N-acetyl cysteine have effectiveness ratings for specific conditions, but the product as a whole lacks proven effectiveness as a liver supplement. Talk with your doctor about whether it makes sense for your needs.
Can I take this if I'm pregnant?
No. Several ingredients—barberry, schisandra, bupleurum, dandelion, and scute—should be avoided during pregnancy due to insufficient safety data or specific safety concerns. Kudzu also advises against use. Talk with your doctor before considering this product during pregnancy.
What are the most common side effects I might experience?
Common side effects from acetyl-L-carnitine include agitation, dry mouth, headache, insomnia, and reduced appetite. N-acetyl cysteine may cause diarrhea, dry mouth, heartburn, nausea, and vomiting. Turmeric can cause constipation, diarrhea, nausea, and vomiting. Most adverse effects are mild and gastrointestinal.
Why does this product interact with so many medications?
Many of the ingredients affect how your liver breaks down drugs (cytochrome P450 enzymes) or how blood clots, or they affect blood pressure or blood sugar. Because the product contains 13 active ingredients, the number of possible medication interactions adds up quickly across all of them.
Is it safe to take this with my blood thinner?
No, not without checking first. Multiple ingredients—acetyl-L-carnitine, N-acetyl cysteine, turmeric, barberry, grapeseed, bupleurum, dandelion, scute, and kudzu—have documented interactions with blood thinners and can increase bleeding risk. Talk with your doctor or pharmacist before using this product if you take any anticoagulant or antiplatelet drug.
Can I take this while breastfeeding?
Several ingredients—acetyl-L-carnitine, barberry, schisandra, bupleurum, dandelion, and scute—advise against breastfeeding use due to insufficient safety information. Milk thistle advises caution. Talk with your doctor or pharmacist before using this product while nursing.

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

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Label information is sourced from the NIH Dietary Supplement Label Database and reflects the product version on file; always read your actual product label. This page is for education only and is not a substitute for professional medical advice. Confirm with your pharmacist or doctor before combining supplements and medications.

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Go deeper

The Full Monographs Behind Liver Optima’s Ingredients

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

Herb & supplement monograph

Acetyl-l-carnitine

Interacts with 203 drugs

Acetyl-L-carnitine is a form of the amino acid carnitine that the body uses to help produce energy in cells. It is most studied for nerve pain and memory-related conditions, though the evide...

Read the full Acetyl-l-carnitine monograph →
Herb & supplement monograph

N-acetyl Cysteine (nac)

Interacts with 294 drugs

N-acetyl cysteine (NAC) is a supplement form of the amino acid cysteine and a building block for the antioxidant glutathione. It has well-established prescription uses for acetaminophen over...

Read the full N-acetyl Cysteine (nac) 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

European Barberry

Interacts with 1,210 drugs

European barberry is a shrub whose root, bark, and berries contain berberine, a bitter plant alkaloid that has been studied mostly in isolated form. Some early research on berberine is promi...

Read the full European Barberry monograph →
Herb & supplement monograph

Schisandra

Interacts with 803 drugs

Schisandra is a traditional Chinese medicine berry used as an adaptogen for stress, fatigue, and liver support. Human evidence is limited and most claims are not well proven, but it appears...

Read the full Schisandra monograph →
Herb & supplement monograph

Methionine

Methionine is an essential amino acid that your body needs for protein building and many basic chemical reactions. Most people get enough from a normal diet, and supplements are generally no...

Read the full Methionine monograph →
Herb & supplement monograph

Milk Thistle

Interacts with 954 drugs

Milk thistle is a popular herbal supplement most often used for liver health, and its main active component is a group of compounds called silymarin. While it is generally well tolerated, th...

Read the full Milk Thistle monograph →
Herb & supplement monograph

Grape

Interacts with 910 drugs

Grapes and grape products like grape seed extract contain antioxidant compounds such as resveratrol and proanthocyanidins that may support heart and blood vessel health. While the food is he...

Read the full Grape monograph →
Herb & supplement monograph

Bupleurum

Interacts with 327 drugs

Bupleurum (Chai Hu) is a root used in traditional Chinese medicine, usually as part of multi-herb formulas, for liver, digestive, and fever-related complaints. High-quality human evidence fo...

Read the full Bupleurum monograph →
Herb & supplement monograph

Dandelion

Interacts with 457 drugs

Dandelion is a common plant used in food and traditional medicine, often promoted as a natural 'water pill' and digestive aid. Human evidence for these uses is very limited, so its benefits...

Read the full Dandelion monograph →
Herb & supplement monograph

Baikal Skullcap

Interacts with 946 drugs

Baikal skullcap is a traditional Chinese herb (Huang Qin) used for inflammation, allergies, and infections, with active compounds like baicalin and baicalein studied mostly in the lab. Human...

Read the full Baikal Skullcap monograph →
Herb & supplement monograph

Kudzu

Interacts with 584 drugs

Kudzu is a fast-growing vine whose root has long been used in traditional Chinese medicine and is now studied mostly for reducing alcohol intake. Early research is promising for cutting back...

Read the full Kudzu monograph →
Sources

Sources & How We Checked

Liver Optima'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 465 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.

Acetyl-l-carnitine 22 references
  1. Thal LJ, Carta A, Clarke WR, et al. A 1-year multicenter placebo-controlled study of acetyl-L-carnitine in patients with Alzheimer's Disease. Neurology 1996;47:705-11. PubMed
  2. Sano M, Bell K, Cote L, et al. Double-blind parallel design pilot study of acetyl levocarnitine in patients with Alzheimer's Disease. Arch Neurol 1992;49:1137-41. PubMed
  3. Spagnoli A, Lucca U, Menasce G, et al. Long-term acetyl-L-carnitine treatment in Alzheimer's Disease. Neurology 1991;41:1726-32. PubMed
  4. Brooks JO 3rd, Yesavage JA, Carta A, Bravi D. Acetyl L-carnitine slows decline in younger patients with Alzheimer's disease: a reanalysis of a double-blind, placebo-controlled study using the trilinear approach. Int Psychoger 1998;10:193-203. PubMed
  5. Pettegrew JW, Klunk WE, Panchalingam K, et al. Clinical and neurochemical effects of acetyl-L-carnitine in Alzheimer's disease. Neurobiol Aging 1995;16:1-4. PubMed
  6. Rai G, Wright G, Scott L, et al. Double-blind, placebo controlled study of acetyl-l-carnitine in patients with Alzheimer's dementia. Curr Med Res Opin 1990;11:638-47. PubMed
  7. Benvenga S, Ruggeri RM, Russo A, et al. Usefulness of L-carnitine, a naturally occurring peripheral antagonist of thyroid hormone action, in iatrogenic hyperthyroidism: a randomized, double-blind, placebo-controlled clinical trial. J Clin Endocrinol Meta
  8. Montgomery SA, Thal LJ, Amrein R. Meta-analysis of double blind randomized controlled clinical trials of acetyl-L-carnitine versus placebo in the treatment of mild cognitive impairment and mild Alzheimer's disease. Int Clin Psychopharmacol 2003;18:61-71.. PubMed
  9. Martinez E, Domingo P, Roca-Cusachs A. Potentiation of acenocoumarol action by L-carnitine. J Intern Med 1993;233:94.
  10. Hudson S, Tabet N. Acetyl-L-carnitine for dementia. Cochrane Database Syst Rev 2003;2:CD003158.. PubMed
  11. Bachmann HU, Hoffmann A. Interaction of food supplement L-carnitine with oral anticoagulant acenocoumarol. Swiss Med Wkly 2004;134:385. PubMed
  12. De Grandis D, Minardi C. Acetyl-L-carnitine (levacecarnine) in the treatment of diabetic neuropathy. A long-term, randomised, double-blind, placebo-controlled study. Drugs R D 2002;3:223-31. PubMed
  13. 12761 Benvenga S, Amato A, Calvani M, Trimarchi F. Effects of carnitine on thyroid hormone action. Ann N Y Acad Sci 2004;1033:158-67. PubMed
  14. Sima AAF, Calvani M, Mehra M, et al. Acetyl-L-carnitine improves pain, nerve regeneration, and vibratory perception in patients with chronic diabetic neuropathy: An analysis of two randomized, placebo-controlled trials. Diabetes Care 2005;28:89-94.
  15. Youle, M. and Osio, M. A double-blind, parallel-group, placebo-controlled, multicentre study of acetyl L-carnitine in the symptomatic treatment of antiretroviral toxic neuropathy in patients with HIV-1 infection. HIV.Med. 2007;8(4):241-250.
  16. Brennan BP, Jensen JE, Hudson JI, Coit CE, Beaulieu A, Pope HG Jr, Renshaw PF, Cohen BM. A placebo-controlled trial of acetyl-L-carnitine and a-lipoic acid in the treatment of bipolar depression. J Clin Psychopharmacol. 2013 Oct;33(5):627-35.
  17. Ledinek AH, Sajko MC, Rot U. Evaluating the effects of amantadin, modafinil and acetyl-L-carnitine on fatigue in multiple sclerosis--result of a pilot randomized, blind study. Clin Neurol Neurosurg. 2013 Dec;115 Suppl 1:S86-9. PubMed
  18. Martinotti G, Andreoli S, Reina D, Di Nicola M, Ortolani I, Tedeschi D, Fanella F, Pozzi G, Iannoni E, D'Iddio S, Prof LJ. Acetyl-l-Carnitine in the treatment of anhedonia, melancholic and negative symptoms in alcohol dependent subjects. Prog Neuropsychop PubMed
  19. Baek SM, Zheng R, Seo EJ, Hwang DY, Kim BH. Pharmacokinetic comparisons of two acetyl-L-carnitine formulations in healthy Korean volunteers. Int J Clin Pharmacol Ther. 2015;53(11):980-6. PubMed
  20. Goodison G, Overeem K, de Monte V, Siskind D. Mania associated with self-prescribed acetyl-l-carnitine in a man with bipolar I disorder. Australas Psychiatry. 2017;25(1):13-4.
  21. Bruno A, Pandolfo G, Crucitti M, Lorusso S, Zoccali RA, Muscatello MR. Acetyl-L-Carnitine Augmentation of Clozapine in Partial-Responder Schizophrenia: A 12-Week, Open-Label Uncontrolled Preliminary Study. Clin Neuropharmacol. 2016;39(6):277-80. PubMed
  22. Veronese N, Stubbs B, Solmi M, Ajnakina O, Carvalho AF, Maggi S. Acetyl-L-Carnitine Supplementation and the Treatment of Depressive Symptoms: A Systematic Review and Meta-Analysis. Psychosom Med. 2018;80(2):154-9. PubMed

See these in context on the Acetyl-l-carnitine monograph →

N-acetyl Cysteine (nac) 86 references
  1. Ellenhorn MJ, et al. Ellenhorn's Medical Toxicology: Diagnoses and Treatment of Human Poisoning. 2nd ed. Baltimore, MD: Williams & Wilkins, 1997.
  2. Jepsen S, Hansen AB. The influence of N-acetylcysteine on the measurement of prothrombin time and activated partial thromboplastin time in healthy subjects. Scand J Clin Lab Invest 1994;54:543-7. PubMed
  3. van Zandwijk N, Dalesio O, Pastorino U, et al. EUROSCAN, a randomized trial of vitamin A and N-acetylcysteine in patients with head and neck cancer or lung cancer. For the European Organization for Research and Treatment of Cancer Head and Neck and Lung C DOI
  4. Horowitz RS, Dart RC, Jarvie DR, et al. Placental transfer of N-acetylcysteine following human maternal acetaminophen toxicity. J Toxicol Clin Toxicol 1997;35:447-51.
  5. Bailey B, McGuigan MA. Management of anaphylactoid reactions to intravenous N-acetylcysteine. Ann Emerg Med 1998;31:710-5. PubMed
  6. Spiller HA, Krenzelok EP, Grande GA, et al. A prospective evaluation of the effect of activated charcoal before oral N-acetylcysteine in acetaminophen overdose. Ann Emerg Med 1994;23:519-23. PubMed
  7. Ardissino D, Merlini PA, Savonitto S, et al. Effect of transdermal nitroglycerin or N-acetylcysteine, or both, in the long-term treatment of unstable angina pectoris. J Am Coll Cardiol 1997;29:941-7. PubMed
  8. Horowitz JD, Henry CA, Syrjanen ML, et al. Nitroglycerine/N-acetylcysteine in the management of unstable angina pectoris. Eur Heart J 1988;9:95-100. PubMed
  9. Louwerse ES, Weverling GJ, Bossuyt PM, et al. Randomized, double-blind, controlled trial of acetylcysteine in amyotrophic lateral sclerosis. Arch Neurol 1995;52:559-64. PubMed
  10. Wiklund O, Fager G, Andersson A, et al. N-acetylcysteine treatment lowers plasma homocysteine but not serum lipoprotein(a) levels. Atherosclerosis 1996;119:99-106. PubMed
  11. De Flora S, Grassi C, Carati L. Attenuation of influenza-like symptomatology and improvement of cell-mediated immunity with long-term N-acetylcysteine treatment. Eur Respir J 1997;10:1535-41. PubMed
  12. Iversen HK. N-acetylcysteine enhances nitroglycerin-induced headache and cranial arterial responses. Clin Pharmacol Ther 1992;52:125-33. PubMed
  13. Behr J, Maier K, Degenkolb B, et al. Antioxidative and clinical effects of high-dose N-acetylcysteine in fibrosing alveolitis. Adjunctive therapy to maintenance immunosuppression. Am J Respir Crit Care Med 1997;156:1897-901.
  14. Tenenbein PK, Sitar DS, Tenenbein M. Interaction between N-acetylcysteine and activated charcoal: implications for the treatment of acetaminophen poisoning. Pharmacotherapy 2001;21:1331-6.
  15. Arstall MA, Yang J, Stafford I, et al. N-acetylcysteine in combination with nitroglycerin and streptokinase for the treatment of evolving acute myocardial infarction. Safety and biochemical effects. Circulation 1995;92:2855-62.
  16. Estensen RD, Levy M, Klopp SJ, et al. N-acetylcysteine suppression of the proliferative index in the colon of patients with previous adenomatous colonic polyps. Cancer Lett 1999;147:109-14. PubMed
  17. Pela R, Calcagni AM, Subiaco S, et al. N-acetylcysteine reduces the exacerbation rate in patients with moderate to severe COPD. Respiration 1999;66:495-500.. PubMed
  18. Oldemeyer JB, Biddle WP, Wurdeman RL, et al. Acetylcysteine in the prevention of contrast-induced nephropathy after coronary angiography. Am Heart J 2003;146:E23. . PubMed
  19. Ekins BR, Ford DC, Thompson MI, et al. The effect of activated charcoal on N-acetylcysteine absorption in normal subjects. Am J Emerg Med. 1987;5(6):483-7. PubMed
  20. Chamberlain JM, Gorman RL, Oderda GM, Klein-Schwartz W, Klein BL. Use of activated charcoal in a simulated poisoning with acetaminophen: a new loading dose for N-acetylcysteine? Ann Emerg Med. 1993;22(9):1398-402. PubMed
  21. Renzi FP, Donovan JW, Martin TG, Morgan L, Harrison EF. Concomitant use of activated charcoal and N-acetylcysteine. Ann Emerg Med. 1985;14(6):568-72. DOI
  22. North DS, Peterson RG, Krenzelok EP. Effect of activated charcoal administration on acetylcysteine serum levels in humans. Am J Hosp Pharm. 1981;38(7):1022-4. DOI
  23. Loscalzo J. N-Acetylcysteine potentiates inhibition of platelet aggregation by nitroglycerin. J Clin Invest. 1985;76(2):703-8. PubMed
  24. Ruiz FJ, Salom MG, Inglés AC, et al. N-acetyl-L-cysteine potentiates depressor response to captopril and enalaprilat in SHRs. Am J Physiol. 1994;267(3 Pt 2):R767-72. PubMed
  25. Deharo E, Barkan D, Krugliak M, Golenser J, Ginsburg H. Potentiation of the antimalarial action of chloroquine in rodent malaria by drugs known to reduce cellular glutathione levels. Biochem Pharmacol. 2003;66(5):809-17. PubMed
  26. Buckley, N. A., Whyte, I. M., O'Connell, D. L., and Dawson, A. H. Oral or intravenous N-acetylcysteine: which is the treatment of choice for acetaminophen (paracetamol) poisoning? J Toxicol.Clin Toxicol. 1999;37(6):759-767.
  27. Sunman, W., Hughes, A. D., and Sever, P. S. Anaphylactoid response to intravenous acetylcysteine. Lancet 5-16-1992;339(8803):1231-1232. PubMed
  28. Reynard, K., Riley, A., and Walker, B. E. Respiratory arrest after N-acetylcysteine for paracetamol overdose. Lancet 9-12-1992;340(8820):675. PubMed
  29. BERNSTEIN, I. L. and AUSDENMOORE, R. W. IATROGENIC BRONCHOSPASM OCCURRING DURING CLINICAL TRIALS OF A NEW MUCOLYTIC AGENT, ACETYLCYSTEINE. Dis.Chest 1964;46:469-473. PubMed
  30. REAS, H. W. THE USE OF N-ACETYLCYSTEINE IN THE TREATMENT OF CYSTIC FIBROSIS. J Pediatr 1964;65:542-557. PubMed
  31. Bibi, H., Seifert, B., Oullette, M., and Belik, J. Intratracheal N-acetylcysteine use in infants with chronic lung disease. Acta Paediatr. 1992;81(4):335-339. PubMed
  32. Jepsen, S., Herlevsen, P., Knudsen, P., Bud, M. I., and Klausen, N. O. Antioxidant treatment with N-acetylcysteine during adult respiratory distress syndrome: a prospective, randomized, placebo-controlled study. Crit Care Med 1992;20(7):918-923. PubMed
  33. Roes, E. M., Raijmakers, M. T., Boo, T. M., Zusterzeel, P. L., Merkus, H. M., Peters, W. H., and Steegers, E. A. Oral N-acetylcysteine administration does not stabilise the process of established severe preeclampsia. Eur.J Obstet.Gynecol.Reprod.Biol 2006
  34. Spiller, H. A., Winter, M. L., Klein-Schwartz, W., and Bangh, S. A. Efficacy of activated charcoal administered more than four hours after acetaminophen overdose. J Emerg.Med 2006;30(1):1-5. PubMed
  35. Tirouvanziam, R., Conrad, C. K., Bottiglieri, T., Herzenberg, L. A., Moss, R. B., and Herzenberg, L. A. High-dose oral N-acetylcysteine, a glutathione prodrug, modulates inflammation in cystic fibrosis. Proc Natl.Acad.Sci U.S.A 3-21-2006;103(12):4628-463
  36. Niemi, T. T., Munsterhjelm, E., Poyhia, R., Hynninen, M. S., and Salmenpera, M. T. The effect of N-acetylcysteine on blood coagulation and platelet function in patients undergoing open repair of abdominal aortic aneurysm. Blood Coagul.Fibrinolysis 2006;1 PubMed
  37. Komisarof, J. A., Gilkey, G. M., Peters, D. M., Koudelka, C. W., Meyer, M. M., and Smith, S. M. N-acetylcysteine for patients with prolonged hypotension as prophylaxis for acute renal failure (NEPHRON). Crit Care Med 2007;35(2):435-441. PubMed
  38. Grimble, G. K. Adverse gastrointestinal effects of arginine and related amino acids. J Nutr 2007;137(6 Suppl 2):1693S-1701S. PubMed
  39. Berk, M., Copolov, D. L., Dean, O., Lu, K., Jeavons, S., Schapkaitz, I., Anderson-Hunt, M., and Bush, A. I. N-acetyl cysteine for depressive symptoms in bipolar disorder--a double-blind randomized placebo-controlled trial. Biol Psychiatry 9-15-2008;64(6) PubMed
  40. Shahin, A. Y., Hassanin, I. M., Ismail, A. M., Kruessel, J. S., and Hirchenhain, J. Effect of oral N-acetyl cysteine on recurrent preterm labor following treatment for bacterial vaginosis. Int J Gynaecol.Obstet. 2009;104(1):44-48. PubMed
  41. Nigwekar, S. U. and Kandula, P. N-acetylcysteine in cardiovascular-surgery-associated renal failure: a meta-analysis. Ann Thorac.Surg 2009;87(1):139-147. PubMed
  42. Sandilands, E. A. and Bateman, D. N. Adverse reactions associated with acetylcysteine. Clin Toxicol.(Phila) 2009;47(2):81-88. PubMed
  43. Wijeysundera, D. N., Karkouti, K., Rao, V., Granton, J. T., Chan, C. T., Raban, R., Carroll, J., Poonawala, H., and Beattie, W. S. N-acetylcysteine is associated with increased blood loss and blood product utilization during cardiac surgery. Crit Care Me PubMed
  44. Holdiness, M. R. Clinical pharmacokinetics of N-acetylcysteine. Clin Pharmacokinet. 1991;20(2):123-134. PubMed
  45. Dawson, A. H., Henry, D. A., and McEwen, J. Adverse reactions to N-acetylcysteine during treatment for paracetamol poisoning. Med J Aust. 3-20-1989;150(6):329-331.
  46. Rasmussen, J. B. and Glennow, C. Reduction in days of illness after long-term treatment with N-acetylcysteine controlled-release tablets in patients with chronic bronchitis. Eur.Respir.J 1988;1(4):351-355. DOI
  47. Walters, M. T., Rubin, C. E., Keightley, S. J., Ward, C. D., and Cawley, M. I. A double-blind, cross-over, study of oral N-acetylcysteine in Sjogren's syndrome. Scand J Rheumatol.Suppl 1986;61:253-258.
  48. Cato, A., Goldstein, I., and Millman, M. A double-blind parallel study of acetylcysteine-isoproterenol and saline-isoproterenol in patients with chronic obstructive lung disease. J Int Med Res 1977;5(3):175-183. PubMed
  49. Parr, G. D. and Huitson, A. Oral Fabrol (oral N-acetyl-cysteine) in chronic bronchitis. Br.J.Dis.Chest 1987;81(4):341-348.
  50. Dano, G. Bronchospasm caused by acetylcysteine in children with bronchial asthma. Acta Allergol. 1971;26(3):181-190. DOI
  51. Howatt, W. F. and DeMuth, G. R. A double-blind study of the use of acetylcysteine in patients with cystic fibrosis. Univ Mich.Med Cent.J 1966;32(2):82-85.
  52. Millman, M. and Grundon, W. Use of acetylcysteine in bronchial asthma and emphysema. J Asthma Res 1969;6(4):199-209. PubMed
  53. Vale, J. A. and Wheeler, D. C. Anaphylactoid reaction to acetylcysteine. Lancet 10-30-1982;2(8305):988.
  54. Mant, T. G., Tempowski, J. H., Volans, G. N., and Talbot, J. C. Adverse reactions to acetylcysteine and effects of overdose. Br Med J (Clin Res Ed) 7-28-1984;289(6439):217-219. PubMed
  55. Myers, C., Bonow, R., Palmeri, S., Jenkins, J., Corden, B., Locker, G., Doroshow, J., and Epstein, S. A randomized controlled trial assessing the prevention of doxorubicin cardiomyopathy by N-acetylcysteine. Semin.Oncol 1983;10(1 Suppl 1):53-55.
  56. Miller, L. F. and Rumack, B. H. Clinical safety of high oral doses of acetylcysteine. Semin.Oncol 1983;10(1 Suppl 1):76-85.
  57. Boman, G., Backer, U., Larsson, S., Melander, B., and Wahlander, L. Oral acetylcysteine reduces exacerbation rate in chronic bronchitis: report of a trial organized by the Swedish Society for Pulmonary Diseases. Eur J Respir.Dis 1983;64(6):405-415.
  58. Tattersall, A. B., Bridgman, K. M., and Huitson, A. Irish general practice study of acetylcysteine (Fabrol) in chronic bronchitis. J Int Med Res 1984;12(2):96-101. PubMed
  59. Jackson, I. M., Barnes, J., and Cooksey, P. Efficacy and tolerability of oral acetylcysteine (Fabrol) in chronic bronchitis: a double-blind placebo controlled study. J Int Med Res 1984;12(3):198-206. PubMed
  60. Ho, S. W. and Beilin, L. J. Asthma associated with N-acetylcysteine infusion and paracetamol poisoning: report of two cases. Br Med J (Clin Res Ed) 9-24-1983;287(6396):876-877. PubMed
  61. Vale, J. A. and Buckley, B. M. Asthma associated with N-acetylcysteine infusion and paracetamol poisoning. Br Med J (Clin Res Ed) 10-22-1983;287(6400):1223. PubMed
  62. Bateman, D. N., Woodhouse, K. W., and Rawlins, M. D. Adverse reactions to N-acetylcysteine. Hum Toxicol. 1984;3(5):393-398. PubMed
  63. Gervais, S., Lussier-Labelle, F., and Beaudet, G. Anaphylactoid reaction to acetylcysteine. Clin Pharm 1984;3(6):586-587.
  64. Tattersall, A. B., Bridgman, K. M., and Huitson, A. Acetylcysteine (Fabrol) in chronic bronchitis--a study in general practice. J Int Med Res 1983;11(5):279-284. PubMed
  65. Casola, G. and vanSonnenberg, E. Skin damage from acetylcysteine leak during percutaneous abscess drainage. Radiology 1984;152(1):233. PubMed
  66. Aylward, M., Maddock, J., and Dewland, P. Clinical evaluation of acetylcysteine in the treatment of patients with chronic obstructive bronchitis: a balanced double-blind trial with placebo control. Eur.J Respir.Dis.Suppl 1980;111:81-89.
  67. Long-term oral acetylcysteine in chronic bronchitis. a double-blind controlled study. Eur.J Respir.Dis.Suppl 1980;111:93-108.
  68. Chan, T. Y. and Critchley, J. A. Adverse reactions to intravenous N-acetylcysteine in Chinese patients with paracetamol (acetaminophen) poisoning. Hum Exp.Toxicol. 1994;13(8):542-544. PubMed
  69. Hansen, N. C., Skriver, A., Brorsen-Riis, L., Balslov, S., Evald, T., Maltbaek, N., Gunnersen, G., Garsdal, P., Sander, P., Pedersen, J. Z., and . Orally administered N-acetylcysteine may improve general well-being in patients with mild chronic bronchiti
  70. Reid, M. B., Stokic, D. S., Koch, S. M., Khawli, F. A., and Leis, A. A. N-acetylcysteine inhibits muscle fatigue in humans. J Clin Invest 1994;94(6):2468-2474. PubMed
  71. Chirkov, Y. Y. and Horowitz, J. D. N-Acetylcysteine potentiates nitroglycerin-induced reversal of platelet aggregation. J Cardiovasc.Pharmacol 1996;28(3):375-380. PubMed
  72. Hershkovitz, E., Shorer, Z., Levitas, A., and Tal, A. Status epilepticus following intravenous N-acetylcysteine therapy. Isr.J Med Sci 1996;32(11):1102-1104.
  73. Stavem, K. [Anaphylactic reaction to N-acetylcysteine after poisoning with paracetamol]. Tidsskr.Nor Laegeforen. 5-30-1997;117(14):2038-2039.
  74. Walton, N. G., Mann, T. A., and Shaw, K. M. Anaphylactoid reaction to N-acetylcysteine. Lancet 12-15-1979;2(8155):1298. PubMed
  75. Perry, H. E. and Shannon, M. W. Efficacy of oral versus intravenous N-acetylcysteine in acetaminophen overdose: results of an open-label, clinical trial. J Pediatr 1998;132(1):149-152. PubMed
  76. Kory, R. C., Hirsch, S. R., and Giraldo, J. Nebulization of N-acetylcysteine combined with a bronchodilator in patients with chronic bronchitis. A controlled study. Chest 1968;54(6):504-509. PubMed
  77. Nahir, A. M., Scharf, J. M., and Szargel, R. Effects of oral N-acetylcysteine on both ocular and oral manifestations of Sjogren's Syndrome. Curr Ther Res 1989;46:187-192.
  78. Charley, G., Dean, B. S., and Krenzelok, E. P. Oral N-acetylcysteine-induced urticaria: a case report. Vet.Hum Toxicol. 1987;29:477.
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See these in context on the N-acetyl Cysteine (nac) monograph →

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See these in context on the Turmeric monograph →

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Schisandra 26 references
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Methionine 12 references
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Milk Thistle 69 references
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Grape 34 references
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  21. Warinsiriruk P, Tantitham C, Cherdshewasart W, Shobeiri SA, Manonai J. Effects of Pueraria mirifica on vaginal artery vascularization in postmenopausal women with genitourinary syndrome of menopause. Maturitas 2022;160:4-10. PubMed

See these in context on the Kudzu monograph →

Parts of this content are provided by the Therapeutic Research Center, LLC.

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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