Major interaction on record — check this product against your medications before combining. Based on 5 of 11 ingredients. Check your meds →
Dietary supplement

Mpc Prostata Corrector Ingredients & Drug Interactions

by Systemic Formulas Bio Function

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

Mpc Prostata Corrector is a dietary supplement by Systemic Formulas Bio Function with 11 active ingredients. Its ingredients are commonly taken for digestive upset and diarrhea, colds and respiratory infections, sore throat and mouth sores.Based on those ingredients, 1,604 medications have a known interaction with it, the most serious rated major. The ingredients most likely to interact are Gingko, Golden Seal, Echinacea purpurea. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.

HelloPharmacist Scorecard of Mpc Prostata Corrector by Systemic Formulas Bio Function

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

Low disclosure
Ingredient Transparency · database check
Low

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

Why this rating?
  • The label discloses an exact amount for 0 of its 11 active ingredients.
  • “Proprietary Blend” is a proprietary blend — the label gives one combined amount (1,000 mg) without saying how much of each component you get.

Mpc Prostata Corrector contains 11 ingredients, of which we have checked five for interactions and safety: goldenseal, pau d'arco, thyme, echinacea purpurea, and ginkgo. We could not verify the interaction or safety profile of pau d'alho or the proprietary RNA/DNA-based factors (prostate, orchic, thymus, pituitary, and hypothalamus factors) because no safety monographs are on file for them.

The product also contains two inactive ingredients: gelatin and stearic acid, which are the capsule material and a binder.

Does it work?

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

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

Why this rating?
  • The label markets this product for: Nutrition for healthy prostate gland.
  • We looked for evidence on: Benign prostatic hyperplasia (BPH), Prostate health, Urinary flow.
  • The closest evidence on file: Goldenseal is rated "Insufficient Reliable Evidence To Rate" for Urinary tract infections (UTIs) (Natural Medicines).
  • Also on file: Echinacea is rated "Insufficient Reliable Evidence To Rate" for Urinary tract infections (UTIs).

The data we hold do not establish that the active ingredients in this product are effective for any particular condition. Goldenseal, pau d'arco, thyme, echinacea, and ginkgo all carry effectiveness ratings of 'Insufficient Reliable Evidence To Rate' for the uses listed in the product's facts.

While ginkgo does show 'Possibly Effective' ratings for hearing loss, stroke, dementia, schizophrenia, premenstrual syndrome, and anxiety in the monograph data, no claim appears in the product facts for any of these uses. If you're considering this product for a specific health goal, talk with your doctor or pharmacist about what the evidence actually shows.

The evidence, ingredient by ingredient Goldenseal Pau D'arco Thyme Echinacea Ginkgo

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 5 of the 5 matched ingredients.
  • Pregnancy & breastfeeding safety ratings cover 5 of 5.
  • General safety write-ups exist for 5 of 5.
  • Remember: this measures how much safety information exists. Thin data is not the same as being safe.

Goldenseal, pau d'arco, and ginkgo each advise against use in pregnancy due to potential harm to the developing baby. Thyme is rated Likely Safe during pregnancy and lactation when used in food amounts, but medicinal doses lack safety data.

The product advises against pau d'arco and ginkgo while breastfeeding due to insufficient safety information. Goldenseal is not recommended while breastfeeding because berberine (its active constituent) may pass to the infant and cause harm.

Echinacea is rated Possibly Safe in pregnancy but has no lactation rating on file. Common side effects from the checked ingredients may include digestive upset (abdominal pain, diarrhea, constipation, nausea, vomiting), headache, dizziness, and heartburn.

Goldenseal and pau d'arco can cause these at higher doses. Echinacea is generally well tolerated but may trigger allergic reactions, especially in people sensitive to ragweed.

Ginkgo is generally well tolerated but may raise bleeding risk and has rarely been linked to cardiac rhythm problems. Thyme is well tolerated in food and medicinal amounts, though topical use can rarely cause contact dermatitis.

Side effects, ingredient by ingredient Goldenseal Pau D'arco Thyme Echinacea Ginkgo

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?
  • 5 of the 5 matched ingredients can interact with medications — Ginkgo, Pau D'arco, Thyme, Goldenseal, Echinacea.
  • The most serious interaction on file is rated Major.
  • Some involve high-stakes drug classes: anticoagulant / antiplatelet drugs; seizure medications; immunosuppressants / transplant drugs; diabetes medications; heart-rhythm medications.
  • For scale: 1,605 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 this product, double-check with your doctor or pharmacist if you're on blood thinners or antiplatelet drugs (warfarin, aspirin, clopidogrel), heart and blood pressure medications (talinolol, alprazolam, simvastatin, antihypertensives, CNS depressants), diabetes drugs, immunosuppressants, liver-metabolized medications (especially those processed by CYP2D6, CYP2C9, CYP3A4, or CYP1A2), HIV protease inhibitors or antiretrovirals (efavirenz), immunosuppressants (tacrolimus), or anticholinergic or cholinergic drugs. The Major interaction with talinolol and the many Moderate interactions across these categories mean your prescriptions need individual review.

Check your own medication Run your meds through the checker above

The bottom line

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

This product combines several herbal ingredients with documented medication interactions, most notably ginkgo's Major interaction with talinolol and multiple Moderate interactions across blood thinners, diabetes drugs, brain medications, and liver enzyme substrates. If you take any prescription medication—especially blood thinners, heart or blood pressure drugs, diabetes medication, immunosuppressants, or drugs that affect the liver—you need to check your exact medications against the tool on this page before starting.

Pregnant or breastfeeding individuals should avoid goldenseal, pau d'arco, and ginkgo. Talk with your doctor or pharmacist about whether this product is right for you and your specific health situation.

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

Assessment coverage: 5 of 11 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated May 24, 2013.

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 Mpc Prostata Corrector, straight from the product label.

Brand Systemic Formulas Bio Function
Barcode (UPC) 635585007214
Net contents 60 Capsule(s)
Market status On market
Date entered into DSLD May 24, 2013
DSLD ID 21956
Product type Other Combinations
Supplement form Capsule
Dietary claims / uses All Other, Structure/Function
Intended target group(s) Adult Male (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 Mpc Prostata Corrector by Systemic Formulas Bio Function, sourced from the NIH Dietary Supplement Label Database.

Supplement Facts

Daily Value (DV) Target Group(s):
Adults and children 4 or more years of age
Minimum serving Sizes:
1 Capsule(s)
Maximum serving Sizes:
2 Capsule(s)
UPC/BARCODE
635585007214
IngredientAmount% DV
Golden Seal0 NP--
Proprietary Blend1000 mg--
Pau d'Arco0 NP--
Thyme0 NP--
Echinacea purpurea0 NP--
RNA/DNA Prostate Factors0 NP--
Gingko0 NP--
Pau d' Alho0 NP--
RNA/DNA Orchic Factors0 NP--
RNA/DNA Thymus Factors0 NP--
RNA/DNA Pituitary Factors0 NP--
RNA/DNA Hypothalamus Factors0 NP--

Other ingredients: Gelatin, Stearic Acid

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.
Storage

Keep away from Heat and Sunlight

General Statements

Nutrition for a healthy prostate gland; provides feelings of well being.

SOLD THROUGH PROFESSIONALS

MADE IN U.S.A.

FDA Disclaimer Statement

This statement has not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent any diseases.

Suggested/Recommended/Usage/Directions

DIRECTIONS FOR NUTRITIONAL USE: 1-2 capsules up to twice a day for 1-6 months, or as directed. Then, take as needed for maintenance. Increase the amount of liquids you drink each day while taking this product.

General

#72 L/9

FDA Statement of Identity

Dietary Supplement

Precautions

KEEP OUT OF REACH OF CHILDREN.

See for yourself

Mpc Prostata Corrector by Systemic Formulas Bio Function label

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

What’s inside

The Ingredients in Mpc Prostata Corrector by Systemic Formulas Bio Function

These are the 11 active ingredients this product is made of. Select any to open its full monograph.

Serving size1 Capsule(s) Dosage formCapsule 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.

Proprietary Blend

1000 mg per serving

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

Interaction report

Mpc Prostata Corrector by Systemic Formulas Bio Function Drug Interactions

Want to check YOUR meds against Mpc Prostata Corrector?

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
1,604Drugs
1 Major 1,601 Moderate 2 Minor

Ingredients driving the most interactions

Gingko 1,266
Golden Seal 1,237
Thyme 379

Each ingredient & the kinds of drugs it affects

For each ingredient in Mpc Prostata Corrector 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.

Gingko23 drug types · 1,266 drugs

Talinolol

Taking ginkgo with talinolol seems to increase blood levels of talinolol.
There is some evidence that using ginkgo leaf extract 120 mg orally three times daily for 14 days can increase levels of talinolol by 36% in healthy male individuals. However, single doses of ginkgo do not seem to affect talinolol pharmacokinetics.

Likelihood Probable Evidence B
Alprazolam (Xanax)

Theoretically, ginkgo might decrease the levels and clinical effects of alprazolam.
In clinical research, ginkgo extract (Ginkgold) 120 mg twice daily seems to decrease alprazolam levels by about 17%. However, ginkgo does not appear to decrease the elimination half-life of alprazolam. This suggests that ginkgo is more likely to decrease absorption of alprazolam rather than induce hepatic metabolism of alprazolam.

Likelihood Probable Evidence B
Anticoagulant/Antiplatelet Drugs

Ginkgo has been shown to increase the risk of bleeding in some people when taken with warfarin. Theoretically, ginkgo might increase the risk of bleeding if used with other anticoagulant or antiplatelet drugs.
Several pharmacodynamic studies suggest that ginkgo inhibits platelet aggregation. It is thought that the ginkgo constituent, ginkgolide B, displaces platelet-activating factor (PAF) from its binding sites, decreasing blood coagulation. Several case reports have documented serious bleeding events in patients taking ginkgo. However, population and clinical studies have produced mixed results. Some evidence shows that short-term use of ginkgo leaf does not significantly reduce platelet aggregation and blood clotting. A study in healthy males who took a specific ginkgo leaf extract (EGb 761) 160 mg twice daily for 7 days found no change in prothrombin time. An analysis of a large medical record database suggests that ginkgo increases the risk of a bleeding adverse event by 38% when taken concurrently with warfarin. It has been suggested that ginkgo has to be taken for at least 2-3 weeks to have a significant effect on platelet aggregation. However, a meta-analysis of 18 studies using standardized ginkgo extracts, 80-480 mg daily for up to 32 weeks, did not find a significant effect on platelet aggregation, fibrinogen concentration, or PT/aPTT. In addition, a single dose of ginkgo plus clopidogrel or ticlopidine does not seem to significantly increase bleeding time or platelet aggregation. Also, taking ginkgo leaf extract daily for 8 days in conjunction with rivaroxaban does not affect anti-factor Xa activity; however, this study did not evaluate bleeding time.

Likelihood Possible Evidence A
Anticonvulsants

Theoretically, ginkgo might reduce the effectiveness of anticonvulsants.
Ginkgo seeds contain ginkgotoxin. Large amounts of ginkgotoxin can cause neurotoxicity and seizure. Ginkgotoxin is present in much larger amounts in ginkgo seeds than leaves. Ginkgo leaf extract contains trace amounts of ginkgotoxin. The amount of ginkgotoxin in ginkgo leaf and leaf extract seems unlikely to cause toxicity. However, there are anecdotal reports of seizure occurring after use of ginkgo leaf both in patients without a history of seizure disorder and in those with previously well-controlled epilepsy.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, taking ginkgo with antidiabetes drugs might alter the response to antidiabetes drugs.
Ginkgo leaf extract seems to alter insulin secretion and metabolism, and might affect blood glucose levels in people with type 2 diabetes. The effect of ginkgo seems to differ depending on the insulin and treatment status of the patient. In diet-controlled diabetes patients with hyperinsulinemia, taking ginkgo does not seem to significantly affect insulin or blood glucose levels. In patients with hyperinsulinemia who are treated with oral hypoglycemic agents, taking ginkgo seems to decrease insulin levels and increase blood glucose following an oral glucose tolerance test. Researchers speculate that this could be due to ginkgo-enhanced hepatic metabolism of insulin. In patients with pancreatic exhaustion, taking ginkgo seems to stimulate pancreatic beta-cells, resulting in increased insulin and C-peptide levels, but with no significant change in blood glucose levels in response to an oral glucose tolerance test.

Likelihood Possible Evidence B
Atorvastatin (Lipitor)

Theoretically, ginkgo might decrease the levels and clinical effects of atorvastatin.
In humans, intake of ginkgo extract appears to increase atorvastatin clearance, reducing the area under the curve of atorvastatin by 10% to 14% and the maximum concentration by 29%. However, this interaction does not appear to affect cholesterol synthesis and absorption. Further, a model in rats with hyperlipidemia suggests that administering ginkgo extract does not impact blood levels of atorvastatin and leads to lower total cholesterol, low-density lipoprotein cholesterol, and triglycerides when compared with rats given atorvastatin alone.

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

Theoretically, ginkgo might increase levels of drugs metabolized by CYP1A2.
Laboratory research suggests that ginkgo leaf extract can mildly inhibit CYP1A2 enzymes. However, clinical research suggests ginkgo might not affect CYP1A2. Until more is known, use ginkgo cautiously in patients taking drugs metabolized by these enzymes.

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

Theoretically, ginkgo might decrease levels of drugs metabolized by CYP2C19.
Some clinical research shows that a specific ginkgo leaf extract (Remembrance, Herbs Product LTD) 140 mg twice daily can induce CYP2C19 enzymes and potentially decrease levels of drugs metabolized by these enzymes. However, other clinical research shows that taking ginkgo 120 mg twice daily for 12 days has no effect on levels of drugs metabolized by CYP2C19.

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

Theoretically, ginkgo might increase levels of drugs metabolized by CYP2C9.
In vitro, a specific standardized extract of ginkgo leaf (EGb 761) inhibits CYP2C9 activity . The terpenoid (ginkgolides) and flavonoid (quercetin, kaempferol, etc.) constituents seem to be responsible for this effect. Most ginkgo extracts contain some amount of these constituents. Therefore, other ginkgo leaf extracts might also inhibit the CYP2C9 enzyme. However, clinical research suggests that ginkgo might not have a significant effect on CYP2C9 in humans. Ginkgo does not seem to significantly affect the pharmacokinetics of CYP2C9 substrates diclofenac or tolbutamide.

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

Theoretically, ginkgo might decrease levels of drugs metabolized by CYP3A4.
There is conflicting evidence about whether ginkgo induces or inhibits CYP3A4. Ginkgo does not appear to affect hepatic CYP3A4. However, it is not known if ginkgo affects intestinal CYP3A4. Preliminary clinical research suggests that taking ginkgo does not significantly affect levels of donepezil, lopinavir, or ritonavir, which are all CYP3A4 substrates. Other clinical research also suggests ginkgo does not significantly affect CYP3A4 activity. However, there are two case reports of decreased efavirenz concentrations and increased viral load in patients taking ginkgo. It is suspected that terpenoids from the ginkgo extract reduced drug levels by inducing cytochrome P450 3A4 (CYP3A4).

Likelihood Possible Evidence B
Efavirenz (Sustiva)

Theoretically, ginkgo might decrease the levels and clinical effects of efavirenz.
There are two case reports of decreased efavirenz concentrations and increased viral load in patients taking ginkgo. In one case, an HIV-positive male experienced over a 50% decrease in efavirenz levels over the course of 14 months while taking ginkgo extract. HIV-1 RNA copies also increased substantially, from less than 50 to more than 1500. It is suspected that terpenoids from the ginkgo extract reduced drug levels by inducing cytochrome P450 3A4 (CYP3A4). In another case report, a patient stable on antiviral therapy including efavirenz for 10 years, had an increase in viral load from <50 copies/mL to 1350 copies/mL after 2 months of taking a combination of supplements including ginkgo. After stopping ginkgo, the viral load was again controlled with the same antiviral therapy regimen.

Likelihood Possible Evidence D
Ibuprofen (Advil, Others)

Theoretically, ginkgo might increase the risk of bleeding when used with ibuprofen.
Ginkgo might have antiplatelet effects and has been associated with several case reports of spontaneous bleeding. In one case, a 71-year-old male had taken a specific ginkgo extract (Gingium, Biocur) 40 mg twice daily for 2.5 years. About 4 weeks after starting ibuprofen 600 mg daily he experienced a fatal intracerebral hemorrhage. However, the antiplatelet effects of ginkgo have been questioned. A meta-analysis and other studies have not found a significant antiplatelet effect with standardized ginkgo extracts, 80 mg to 480 mg taken daily for up to 32 weeks.

Likelihood Possible Evidence D
P-Glycoprotein Substrates

Theoretically, taking ginkgo with P-glycoprotein substrates might increase the levels and adverse effects of these substrates.
A small clinical study in healthy volunteers shows that using ginkgo leaf extract 120 mg orally three times daily for 14 days can increase levels of the P-glycoprotein substrate, talinolol, by 36% in healthy male individuals. However, single doses of ginkgo do not have the same effect.

Likelihood Possible Evidence B
Risperidone (Risperdal)

Theoretically, taking ginkgo with risperidone might increase the levels and adverse effects of risperidone.
A single case of priapism has been reported for a 26-year-old male with schizophrenia who used risperidone 3 mg daily along with ginkgo extract 160 mg daily. Risperidone is metabolized by cytochrome P450 (CYP) 2D6 and CYP3A4. CYP3A4 activity might be affected by ginkgo. Theoretically, ginkgo may inhibit the metabolism of risperidone and increase the risk of adverse effects.

Likelihood Possible Evidence D
Rosiglitazone (Avandia)

Theoretically, ginkgo might decrease the levels and clinical effects of rosiglitazone.
Animal research shows that ginkgo leaf extract orally 100 or 200 mg/kg daily for 10 days alters the pharmacodynamics of rosiglitazone in a dose-dependent manner. The 100 mg/kg and 200 mg/kg doses reduce the area under the concentration time curve (AUC) of rosiglitazone by 39% and 52%, respectively, and the half-life by 28% and 39%, respectively. It is hypothesized that these changes may be due to induction of cytochrome P450 2C8 by ginkgo.

Likelihood Possible Evidence D
Seizure Threshold Lowering Drugs

Theoretically, taking ginkgo with drugs that lower the seizure threshold might increase the risk for convulsions.
Ginkgo seeds contain ginkgotoxin. Large amounts of ginkgotoxin can cause neurotoxicity and seizure. Ginkgotoxin is present in much larger amounts in ginkgo seeds than leaves. Ginkgo leaf extract contains trace amounts of ginkgotoxin. The amount of ginkgotoxin in ginkgo leaf and leaf extract seems unlikely to cause toxicity. However, there are anecdotal reports of seizure occurring after use of ginkgo leaf both in patients without a history of seizure disorder and in those with previously well-controlled epilepsy.

Likelihood Possible Evidence D
Simvastatin (Zocor)

Theoretically, ginkgo might decrease the levels and clinical effects of simvastatin.
Clinical research shows that taking ginkgo extract can reduce the area under the curve and maximum concentration of simvastatin by 32% to 39%. However, ginkgo extract does not seem to affect the cholesterol-lowering ability of simvastatin.

Likelihood Probable Evidence B
Sofosbuvir (Sovaldi)

Theoretically, ginkgo might increase the levels and clinical effects of sofosbuvir.
Animal research in rats shows that giving a ginkgo extract 25 mg/kg orally daily for 14 days increases the area under the concentration time curve (AUC) after a single sofosbuvir dose of 40 mg/kg by 11%, increases the half-life by 60%, and increases the plasma concentration at 4 hours by 38%. This interaction appears to be related to the inhibition of intestinal P-glycoprotein by ginkgo.

Likelihood Possible Evidence D
Tacrolimus (Prograf)

Theoretically, ginkgo might increase the blood levels of tacrolimus.
In vitro evidence suggests that certain biflavonoids in ginkgo leaves (i.e. amentoflavone, ginkgetin, bilobetin) may inhibit the metabolism of tacrolimus by up to 50%. This interaction appears to be time-dependent and due to inhibition of cytochrome P450 (CYP) 3A4 by these bioflavonoids. In rats given tacrolimus 1 mg/kg orally, amentoflavone was shown to increase the area under the concentration time curve (AUC) of tacrolimus by 3.8-fold.

Likelihood Possible Evidence D
Trazodone (Desyrel)

Theoretically, ginkgo might increase the levels and clinical effects of trazodone.
In a case report, an Alzheimer patient taking trazodone 20 mg twice daily and ginkgo leaf extract 80 mg twice daily for four doses became comatose. The coma was reversed by administration of flumazenil (Romazicon). Coma might have been induced by excessive GABA-ergic activity. Ginkgo flavonoids are thought to have GABA-ergic activity and act directly on benzodiazepine receptors. Ginkgo might also increase metabolism of trazodone to active GABA-ergic metabolites, possibly by inducing cytochrome P450 3A4 (CYP3A4) metabolism.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Ginkgo has been shown to increase the risk of bleeding in some people when taken with warfarin.
Several pharmacodynamic studies suggest that ginkgo inhibits platelet aggregation. It is thought that the ginkgo constituent, ginkgolide B, displaces platelet-activating factor (PAF) from its binding sites, decreasing blood coagulation. Several case reports have documented serious bleeding events in patients taking ginkgo. Information from a medical database suggests that when taken concurrently with warfarin, ginkgo increases the risk of a bleeding adverse event by 38%. There is also some evidence that ginkgo leaf extract can inhibit cytochrome P450 2C9, an enzyme that metabolizes warfarin. This could result in increased warfarin levels. However, population and clinical research has produced mixed results. Clinical research in healthy people suggests that ginkgo has no effect on INR, or the pharmacokinetics or pharmacodynamics of warfarin. A meta-analysis of 18 studies using standardized ginkgo extracts, 80 mg to 480 mg daily for up to 32 weeks, did not find a significant effect on platelet aggregation, fibrinogen concentration, or PT/aPTT. There is also some preliminary clinical research that suggests ginkgo might not significantly increase the effects of warfarin in patients that have a stable INR.

Likelihood Possible Evidence B
Nifedipine (Procardia)

Theoretically, taking ginkgo with oral, but not intravenous, nifedipine might increase levels and adverse effects of nifedipine.
Animal research and some clinical evidence suggests that taking ginkgo leaf extract orally in combination with oral nifedipine might increase nifedipine levels and cause increased side effects, such as headaches, dizziness, and hot flushes. However, taking ginkgo orally does not seem to affect the pharmacokinetics of intravenous nifedipine.

Likelihood Possible Evidence B
Omeprazole (Prilosec)

Theoretically, taking ginkgo with omeprazole might decrease the levels and clinical effects of omeprazole.
Clinical research shows that a specific ginkgo leaf extract (Remembrance, Herbs Product LTD) 140 mg twice daily can induce cytochrome P450 (CYP) 2C19 enzymes and decrease levels of omeprazole by about 27% to 42%.

Likelihood Possible Evidence B

Golden Seal16 drug types · 1,237 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, goldenseal might increase the risk of bleeding when used with anticoagulant or antiplatelet drugs.
Goldenseal contains berberine. In vitro and animal research shows that berberine can inhibit platelet aggregation. However, this effect has not been reported in humans.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, goldenseal might increase the risk of hypoglycemia when used with antidiabetes drugs.
Goldenseal contains berberine. Clinical research shows that berberine can lower blood glucose levels. However, this effect has not been reported with goldenseal.

Likelihood Possible Evidence D
Antihypertensive Drugs

Theoretically, goldenseal might increase the risk of hypotension when taken with antihypertensive drugs.
Goldenseal contains berberine. Animal research shows that berberine can have hypotensive effects. Also, an analysis of clinical research shows that taking berberine in combination with amlodipine can lower systolic and diastolic blood pressure when compared with amlodipine alone. However, this effect has not been reported with goldenseal.

Likelihood Possible Evidence D
Cns Depressants

Theoretically, goldenseal might increase the sedative effects of CNS depressants.
Goldenseal contains berberine. Animal research shows that berberine can have sedative effects. However, this effect has not been reported in humans.

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

Theoretically, goldenseal might increase serum levels of drugs metabolized by CYP2C9.
In vitro research shows that goldenseal root extract can modestly inhibit CYP2C9. This effect may be due to its alkaloid constituents, hydrastine and berberine. However, this effect has not been reported in humans.

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

Goldenseal might increase serum levels of drugs metabolized by CYP2D6.
Clinical and in vitro research shows that goldenseal can significantly inhibit CYP2D6 enzymes, potentially increasing levels of drugs metabolized by CYP2D6.

Likelihood Probable Evidence B
Cytochrome P450 2E1 (Cyp2E1) Substrates

Theoretically, goldenseal might increase serum levels of drugs metabolized by CYP2E1.
In vitro research shows that goldenseal root extract can inhibit the activity of CYP2E1. However, this effect has not been reported in humans.

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

Goldenseal might increase serum levels of drugs metabolized by CYP3A4.
Most clinical and in vitro research shows that goldenseal inhibits CYP3A4 enzyme activity and increases serum levels of CYP3A4 substrates, such as midazolam. However, in one small clinical study, goldenseal did not affect the levels of indinavir, a CYP3A4 substrate, in healthy volunteers. This is likely due to the fact that indinavir has a high oral bioavailability, making it an inadequate probe for CYP3A4 interactions and/or that it is primarily metabolized by hepatic CYP3A, while goldenseal has more potential to inhibit intestinal CYP3A enzyme activity. Both goldenseal extract and its isolated constituents berberine and hydrastine inhibit CYP3A, with hydrastine possibly having more inhibitory potential than berberine.

Likelihood Possible Evidence B
Dextromethorphan (Robitussin Dm, Others)

Theoretically, goldenseal might increase serum levels of dextromethorphan.
Goldenseal contains berberine. A small clinical study shows that berberine can inhibit cytochrome P450 2D6 (CYP2D6) activity and reduce the metabolism of dextromethorphan.

Likelihood Possible Evidence D
Digoxin (Lanoxin)

Goldenseal might increase serum levels of digoxin, although this effect is unlikely to be clinically significant.
Clinical research shows that goldenseal modestly increases digoxin peak levels by about 14% in healthy volunteers. However, goldenseal does not seem to affect other pharmacokinetic parameters such as area under the curve (AUC). This suggests that goldenseal does not cause a clinically significant interaction with digoxin. Digoxin is a P-glycoprotein substrate. Some evidence suggests that goldenseal constituents might affect P-glycoprotein; however, it is unclear whether these constituents inhibit or induce P-glycoprotein.

Likelihood Probable Evidence B
Losartan (Cozaar)

Theoretically, goldenseal might decrease the conversion of losartan to its active form.
Goldenseal contains berberine. A small clinical study shows that berberine inhibits cytochrome P450 2C9 (CYP2C9) activity and reduces the metabolism of losartan. However, this effect has not been reported with goldenseal.

Likelihood Possible Evidence D
Metformin (Glucophage)

Theoretically, goldenseal might reduce blood levels of metformin.
In vitro research shows that goldenseal extract decreases the bioavailability of metformin, likely by interfering with transport, intestinal permeability, or other processes involved in metformin absorption. It is unclear which, if any, of metformin's transporters are inhibited by goldenseal. Goldenseal does not appear to alter the clearance or half-life of metformin.

Likelihood Possible Evidence D
P-Glycoprotein Substrates

Theoretically, goldenseal might increase or decrease serum levels of P-glycoprotein (P-gp) substrates.
There is conflicting evidence about the effect of goldenseal on P-gp. In vitro research suggests that berberine, a constituent of goldenseal, modestly inhibits P-gp efflux. Other evidence suggests that berberine induces P-gp. In healthy volunteers, goldenseal modestly increases peak levels of the P-gp substrate digoxin by about 14%. However, it does not seem to affect other pharmacokinetic parameters such as area under the curve (AUC). This suggests that goldenseal is not a potent inhibitor of P-gp-mediated drug efflux. Until more is known, goldenseal should be used cautiously with P-gp substrates.

Likelihood Probable Evidence B
Pentobarbital (Nembutal)

Theoretically, goldenseal might increase the sedative effects of pentobarbital.
Animal research shows that berberine, a constituent of goldenseal, can prolong pentobarbital-induced sleeping time. However, this effect has not been reported with goldenseal.

Likelihood Possible Evidence D
Tacrolimus (Prograf)

Theoretically, goldenseal might increase serum levels of tacrolimus.
Goldenseal contains berberine. In a 16-year-old patient with idiopathic nephrotic syndrome who was being treated with tacrolimus 6.5 mg twice daily, intake of berberine 200 mg three times daily increased the blood concentration of tacrolimus from 8 to 22 ng/mL. Following a reduction of tacrolimus dosing to 3 mg daily, blood levels of tacrolimus decreased to 12 ng/mL.

Likelihood Possible Evidence D
Oseltamivir (Tamiflu)

Theoretically, goldenseal might reduce the therapeutic effects of oseltamivir by decreasing its conversion to its active form.
In vitro evidence suggests that goldenseal reduces the formation of the active compound from the prodrug oseltamivir. The mechanism of action and clinical relevance is unclear.

Likelihood Possible Evidence D

Echinacea purpurea12 drug types · 816 drugs

Caffeine

Echinacea can increase plasma levels of caffeine by inhibiting its metabolism.
Echinacea seems to increase plasma concentrations of caffeine by around 30%. This is likely due to inhibition of cytochrome P450 1A2 (CYP1A2) by echinacea.

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

Echinacea might inhibit the metabolism of CYP1A2 and increase plasma levels of some drugs.
Echinacea appears to inhibit CYP1A2 enzymes in humans. Additionally, echinacea seems to increase plasma concentrations of caffeine, a CYP1A2 substrate, by around 30%. Theoretically, echinacea might increase levels of other drugs metabolized by CYP1A2.

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

Echinacea may induce hepatic CYP3A4 and inhibit intestinal CYP3A4. This may increase or decrease levels of drugs metabolized by CYP3A4.
Several clinical trials have shown that taking echinacea for up to one month does not significantly affect the metabolism of various CYP3A4 substrates, including midazolam, docetaxel, etravirine, lopinavir-ritonavir, and darunavir-ritonavir. However, other clinical research shows that echinacea may increase the clearance of midazolam, suggesting that echinacea might induce CYP3A4. The discrepancy is thought to be due to differing effects of echinacea on intestinal versus hepatic CYP3A4 enzymes. Echinacea appears to induce hepatic CYP3A4 but inhibit intestinal CYP3A4. In some cases, these effects might cancel each other out, but in others, drug levels may be increased or decreased depending on the level of effect at hepatic and intestinal sites. The effect of echinacea on CYP3A4 activity may differ depending on the CYP3A4 substrate.

Likelihood Possible Evidence B
Etoposide (Vepesid)

Echinacea may increase levels of etoposide.
In one report, concomitant use of etoposide and echinacea was associated with more severe thrombocytopenia than the use of etoposide alone, suggesting inhibition of etoposide metabolism. Etoposide is a cytochrome P450 3A4 (CYP3A4) substrate. Echinacea has variable effects on CYP3A4, but some studies have reported inhibition of the enzyme.

Likelihood Possible Evidence D
Immunosuppressants

Echinacea has immunostimulant activity which may interfere with immunosuppressant therapy.
Theoretically, echinacea may interfere with immunosuppressant therapy because of its immunostimulant activity.

Likelihood Possible Evidence B
Darunavir (Prezista)

Theoretically, echinacea may interfere with the metabolism of darunavir; however, a small clinical study found no effect.
Darunavir is metabolized by cytochrome P450 3A4 (CYP3A4) and is administered with the CYP3A4 inhibitor ritonavir to increase its plasma concentrations. Echinacea has variable effects on CYP3A4, but administration of an E. purpurea root extract (Arkocapsulas Echinacea, Arkopharma) 500 mg four times daily for 14 days did not affect darunavir/ritonavir pharmacokinetics in 15 HIV-infected patients.

Likelihood Unlikely Evidence B
Dayquil Severe

Echinacea is reported to have varying effects on a number of Cytochrome P450 metabolizing enzymes in the liver, including CYP1A2 and CYP3A4, which play a role in acetaminophen and dextromethorphan metabolism (both contained in DayQuil Severe), respectively. Studies have reported both enzyme inhibition and induction, making it difficult to predict clinically significant drug interactions with reliability. Specific drug interaction studies reporting definitive results are rare, and potential drug interactions involving echinacea should likely be taken on a case-by-case basis. Based on what we know about how acetaminophen and dextromethorphan are metabolized, the risk of a clinically significant interaction between echinacea and DayQuil Severe is low.

Likelihood Unlikely Evidence A
Docetaxel (Taxotere)

Theoretically, echinacea may interfere with the metabolism of docetaxel; however, a small clinical study found no effect.
Docetaxel is metabolized by cytochrome P450 3A4 (CYP3A4). Echinacea has variable effects on CYP3A4, but taking E. purpurea whole plant extract (Echinaforce, A. Vogel Biopharma AG) 20 drops three times daily for 2 weeks did not alter the pharmacokinetics of docetaxel in one clinical study.

Likelihood Unlikely Evidence B
Etravirine (Intelence)

Theoretically, echinacea may interfere with the metabolism of etravirine; however, a small clinical study found no effect.
Etravirine is metabolized by cytochrome P450 3A4 (CYP3A4). Echinacea has variable effects on CYP3A4, but taking E. purpurea root extract (Arkocapsulas Echinacea, Arkopharma) 500 mg three times daily for 14 days did not alter the pharmacokinetics of etravirine in HIV-infected patients.

Likelihood Unlikely Evidence B
Lopinavir/Ritonavir (Kaletra)

Theoretically, echinacea may interfere with the metabolism of lopinavir; however, a small clinical study found no effect.
Lopinavir is metabolized by cytochrome P450 3A4 (CYP3A4) and is administered with the CYP3A4 inhibitor ritonavir to increase its plasma concentrations. Echinacea has variable effects on CYP3A4, but taking E. purpurea (Echinamide, Natural Factors Nutritional Products, Inc.) 500 mg three times daily for 14 days did not alter the pharmacokinetics of lopinavir/ritonavir in healthy volunteers.

Likelihood Unlikely Evidence B
Midazolam (Versed)

Theoretically, echinacea may increase the metabolism of intravenous midazolam.
Echinacea induces hepatic CYP3A4 and might decrease plasma levels of midazolam by about 20%, reducing the effectiveness of intravenous midazolam. Echinacea also appears to inhibit intestinal CYP3A4, which could theoretically increase the bioavailability of oral midazolam. This may cancel out the decrease in availability caused by induction of hepatic CYP3A4, such that overall plasma levels after oral administration of midazolam are not affected by echinacea.

Likelihood Possible Evidence B
Warfarin (Coumadin)

Echinacea seems to increase the clearance of warfarin, although the effect may not be clinically significant.
Preliminary clinical research in healthy male volunteers suggests that taking echinacea increases the clearance of the active S-isomer of warfarin after a single dose of warfarin, but there was not a clinically significant effect on the INR.

Likelihood Possible Evidence B

Thyme4 drug types · 379 drugs

Anticholinergic Drugs

Theoretically, concurrent use of anticholinergic drugs and thyme essential oil might reduce the effects of anticholinergic drugs.
In vitro evidence suggests that thyme essential oil and specific essential oil constituents like thymohydroquinone and carvacrol can inhibit acetylcholinesterase (AChE). However, this effect has not been observed in humans.

Likelihood Possible Evidence D
Anticoagulant/Antiplatelet Drugs

Theoretically, thyme leaf extract might have additive effects with anticoagulant or antiplatelet drugs.
In vitro and animal research suggests that thyme leaf extract has antiplatelet effects. However, this effect has not been observed in humans.

Likelihood Possible Evidence D
Cholinergic Drugs

Theoretically, concurrent use of cholinergic drugs and thyme essential oil might cause additive cholinergic effects.
In vitro evidence suggests that thyme essential oil and specific essential oil constituents like thymohydroquinone and carvacrol can inhibit acetylcholinesterase (AChE). However, this effect has not been observed in humans.

Likelihood Possible Evidence D
Estrogens

Theoretically, thyme might competitively inhibit the effects of estrogen replacement therapy.
In vitro research shows that thyme has estrogen receptor-binding activity and phytoestrogen content. However, this effect has not been observed in humans.

Likelihood Possible Evidence D

Pau d'Arco1 drug type · 122 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, pau d'arco might increase the risk of bleeding when taken with anticoagulant or antiplatelet drugs.
In vitro research shows that pau d'arco reduces platelet aggregation and may interfere with vitamin K. One clinical study shows that taking the lapachol constituent of pau d'arco in doses above 1.5 grams daily increases the risk of bleeding. The effects of whole pau d'arco or pau d'arco extract in humans are unclear.

Likelihood Possible Evidence D
The maker

Brand information

Manufacturer and brand details for Mpc Prostata Corrector, from the product label.

Systemic Formulas Bio Function

See all Systemic Formulas Bio Function products
Name
Systemic Formulas Inc.
Street Address
P.O.Box 1516
City
Ogden
State
UT
ZipCode
84402
Pharmacist Counseling Corner

Mpc Prostata Corrector by Systemic Formulas Bio Function: Common Questions

Does Mpc Prostata Corrector by Systemic Formulas Bio Function interact with any medications?
Yes. Based on its ingredients, Mpc Prostata Corrector has a known interaction with 1,604 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?
Mpc Prostata Corrector contains 11 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.
Can I take this while I'm pregnant or breastfeeding?
No, you should avoid goldenseal, pau d'arco, and ginkgo during pregnancy because the safety data advise against them. Goldenseal and pau d'arco should also be avoided while breastfeeding. Thyme is rated safe in food amounts during pregnancy and breastfeeding, and echinacea is rated Possibly Safe in pregnancy, but medicinal doses of thyme and other ingredients lack sufficient safety data. Talk with your doctor or pharmacist for personalized advice before taking this product.
Is ginkgo in here safe with my blood thinner?
No, ginkgo carries a Moderate-severity risk with blood thinners like warfarin because it may increase bleeding risk. Your doctor or pharmacist needs to review this product against your specific medication before you start it.
What side effects might I experience?
The most common side effects from these ingredients are digestive complaints—nausea, vomiting, diarrhea, constipation, abdominal pain—as well as headache, dizziness, and heartburn. Echinacea may trigger allergic reactions in people sensitive to ragweed. Ginkgo has rarely been linked to irregular heartbeat. If any of these occur, stop taking the product and talk with your pharmacist.
Does this product actually work for prostate health?
The evidence data we hold do not establish that the active ingredients in this product are effective for any specific condition, including prostate health. If you want to know whether these ingredients have any proven benefit for your situation, talk with your doctor or pharmacist.
What are the RNA/DNA ingredients in here?
The product contains several proprietary RNA/DNA-based factors (prostate, orchic, thymus, pituitary, and hypothalamus factors). We don't have safety or interaction data on file for these ingredients, so we cannot tell you whether they're safe or how they may interact with medications. Your pharmacist may have more information.
Can I take this with my diabetes medication?
Theoretically, goldenseal may increase the risk of low blood sugar when used with diabetes drugs, and ginkgo may decrease the effectiveness of rosiglitazone (Avandia). You need to check your specific medication and dose with your doctor or pharmacist before starting this product.

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

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Mpc Prostata Corrector label
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The Full Monographs Behind Mpc Prostata Corrector’s Ingredients

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

Sources

Sources & How We Checked

Mpc Prostata Corrector'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 206 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.

Goldenseal 34 references
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  2. Budzinski JW, Foster BC, Vandenhoek S, Arnason JT. An in vitro evaluation of human cytochrome P450 3A4 inhibition by selected commercial herbal extracts and tinctures. Phytomedicine 2000;7:273-82. PubMed
  3. Sandhu RS, Prescilla RP, Simonelli TM, Edwards DJ. Influence of goldenseal root on the pharmacokinetics of indinavir. J Clin Pharmacol 2003;43:1283-8.. PubMed
  4. Janbaz KH, Gilani AH. Studies on preventive and curative effects of berberine on chemical-induced hepatotoxicity in rodents. Fitoterapia 2000;71:25-33.. PubMed
  5. Gurley BJ, Gardner SF, Hubbard MA, et al. In vivo effects of goldenseal, kava kava, black cohosh, and valerian on human cytochrome P450 1A2, 2D6, 2E1, and 3A4/5 phenotypes. Clin Pharmacol Ther 2005;77:415-26. PubMed
  6. Gurley BJ, Swain A, Barone GW, et al. Effect of goldenseal (Hydrastis canadensis) and kava kava (Piper methysticum) supplementation on digoxin pharmacokinetics in humans. Drug Metab Dispos 2007;35:240-5. PubMed
  7. Gurley BJ, Swain A, Hubbard MA, et al. Clinical assessement of CYP2D6-mediated herb-drug interactions in humans: Effects of milk-thistle, black cohosh, goldenseal, kava kava, St. John's wort, and Echinacea. Mol Nutr Food Res 2008;52:755-63.
  8. Zhang Y, Li X, Zou D, et al. Treatment of type 2 diabetes and dyslipidemia with the natural plant alkaloid berberine. J Clin Endocrinol Metab 2008;93:2559-65. PubMed
  9. Chatterjee P, Franklin MR. Human cytochrome p450 inhibition and metabolic-intermediate complex formation by goldenseal extract and its methylenedioxyphenyl components. Drug Metab Dispos 2003;31:1391-7. PubMed
  10. Choudhry, V. P., Sabir, M., and Bhide, V. N. Berberine in giardiasis. Indian Pediatr. 1972;9(3):143-146.
  11. Shanbhag, S. M., Kulkarni, H. J., and Gaitonde, B. B. Pharmacological actions of berberine on the central nervous system. Jpn.J Pharmacol 1970;20(4):482-487. PubMed
  12. Wu, J. F. and Liu, T. P. [Effects of berberine on platelet aggregation and plasma levels of TXB2 and 6-keto-PGF1 alpha in rats with reversible middle cerebral artery occlusion]. Yao Xue.Xue.Bao. 1995;30(2):98-102.
  13. Peng, W. H., Hsieh, M. T., and Wu, C. R. Effect of long-term administration of berberine on scopolamine-induced amnesia in rats. Jpn J Pharmacol 1997;74(3):261-266. DOI
  14. Sharda DC. Berberine in the treatment of diarrhoea of infancy and childhood. J Indian M A 1970;54(1):22-24.
  15. Sabir M and Bhide NK. Study of some pharmacological actions of berberine. Ind J Physiol & Pharmac 1971;15(3):111-132.
  16. Tripathi YB and Shukla SD. Berberis artistata inhibits PAF induced aggregation of rabbit platelets. Phytotherapy Research 1996;10:628-630.
  17. Zhang, Y., Li, X., Zou, D., Liu, W., Yang, J., Zhu, N., Huo, L., Wang, M., Hong, J., Wu, P., Ren, G., and Ning, G. Treatment of type 2 diabetes and dyslipidemia with the natural plant alkaloid berberine. J Clin Endocrinol.Metab 2008;93(7):2559-2565. PubMed
  18. Yin, J., Xing, H., and Ye, J. Efficacy of berberine in patients with type 2 diabetes mellitus. Metabolism 2008;57(5):712-717. PubMed
  19. Zhang, H., Wei, J., Xue, R., Wu, J. D., Zhao, W., Wang, Z. Z., Wang, S. K., Zhou, Z. X., Song, D. Q., Wang, Y. M., Pan, H. N., Kong, W. J., and Jiang, J. D. Berberine lowers blood glucose in type 2 diabetes mellitus patients through increasing insulin re
  20. Guo, Y., Chen, Y., Tan, Z. R., Klaassen, C. D., and Zhou, H. H. Repeated administration of berberine inhibits cytochromes P450 in humans. Eur J Clin Pharmacol 2012;68(2):213-217. PubMed
  21. Wei, W., Zhao, H., Wang, A., Sui, M., Liang, K., Deng, H., Ma, Y., Zhang, Y., Zhang, H., and Guan, Y. A clinical study on the short-term effect of berberine in comparison to metformin on the metabolic characteristics of women with polycystic ovary syndro
  22. Meng, S., Wang, L. S., Huang, Z. Q., Zhou, Q., Sun, Y. G., Cao, J. T., Li, Y. G., and Wang, C. Q. Berberine ameliorates inflammation in patients with acute coronary syndrome following percutaneous coronary intervention. Clin Exp.Pharmacol Physiol 2012;39 PubMed
  23. Chun YT, Yip TT, Lau KL, and et al. A biochemical study on the hypotensive effect of berberine in rats. Gen Pharmac 1979;10:177-182. PubMed
  24. Sevior, D. K., Hokkanen, J., Tolonen, A., Abass, K., Tursas, L., Pelkonen, O., and Ahokas, J. T. Rapid screening of commercially available herbal products for the inhibition of major human hepatic cytochrome P450 enzymes using the N-in-one cocktail. Xeno PubMed
  25. Bhowmick, S. K., Hundley, O. T., and Rettig, K. R. Severe hypernatremia and hyperosmolality exacerbated by an herbal preparation in a patient with diabetic ketoacidosis. Clin Pediatr (Phila) 2007;46(9):831-834. PubMed
  26. Gurley BJ, et al. Supplementation with goldenseal (Hydrastis canadensis), but not kava kava (Piper methysticum), inhibits human CYP3A activitiy In Vivo. Clin Pharmacol Ther. 2008;83(1):61-69.
  27. Dong H, Zhao Y, Zhao L, Lu F. The effects of berberine on blood lipids: a systemic review and meta-analysis of randomized controlled trials. Planta Med 2013;79(6):437-46. PubMed
  28. Hou Q, Han W, Fu X. Pharmacokinetic interaction between tacrolimus and berberine in a child with idiopathic nephrotic syndrome. Eur J Clin Pharmacol 2013;69(10):1861-2. PubMed
  29. Lan J, Zhao Y, Dong F, et al. Meta-analysis of the effect and safety of berberine in the treatment of type 2 diabetes mellitus, hyperlipemia and hypertension. J Ethnopharmacol. 2015;161:69-81. PubMed
  30. Jalloh MA, Gregory PJ, Hein D, et al. Dietary supplement interactions with antiretrovirals: a systematic review. Int J STD AIDS. 2017 Jan;28(1):4-15. PubMed
  31. Yamaura K, Shimada M, Nakayama N, Ueno K. Protective effects of goldenseal (Hydrastis canadensis L.) on acetaminophen-induced hepatotoxicity through inhibition of CYP2E1 in rats. Pharmacognosy Res. 2011;3(4):250-5. PubMed
  32. Nguyen JT, Tian DD, Tanna RS, et al. Assessing transporter-mediated natural product-drug interactions via in vitro-in vivo extrapolation: clinical evaluation with a probe cocktail. Clin Pharmacol Ther 2021;109(5):1342-52.
  33. Liu R, Tam TW, Mao J, et al. The effect of natural health products and traditional medicines on the activity of human hepatic microsomal-mediated metabolism of oseltamivir. J Pharm Pharm Sci 2010;13(1):43-55. PubMed
  34. Nguyen JT, Tian DD, Tanna RS, et al. An Integrative Approach to Elucidate Mechanisms Underlying the Pharmacokinetic Goldenseal-Midazolam Interaction: Application of In Vitro Assays and Physiologically Based Pharmacokinetic Models to Understand Clinical Ob

See these in context on the Goldenseal monograph →

Pau D'arco 6 references
  1. Gómez Castellanos JR, Prieto JM, Heinrich M. Red Lapacho (Tabebuia impetiginosa)--a global ethnopharmacological commodity? J Ethnopharmacol 2009;121:1-13. PubMed
  2. Guerra, Mde O., Mazoni, A. S., Brandao, M. A., and Peters, V. M. Toxicology of Lapachol in rats: embryolethality. Braz.J Biol. 2001;61(1):171-174. PubMed
  3. Felicio, A. C., Chang, C. V., Brandao, M. A., Peters, V. M., and Guerra, Mde O. Fetal growth in rats treated with lapachol. Contraception 2002;66(4):289-293. PubMed
  4. Son, D. J., Lim, Y., Park, Y. H., Chang, S. K., Yun, Y. P., Hong, J. T., Takeoka, G. R., Lee, K. G., Lee, S. E., Kim, M. R., Kim, J. H., and Park, B. S. Inhibitory effects of Tabebuia impetiginosa inner bark extract on platelet aggregation and vascular s
  5. Block JB, Serpick AA, Miller W, Wiernik PH. Early clinical studies with lapachol (NSC-11905). Cancer Chemother Rep 2. 1974;4(4):27-8.
  6. Algranti E, Mendonça EM, Ali SA, Kokron CM, Raile V. Occupational asthma caused by Ipe (Tabebuia spp) dust. J Investig Allergol Clin Immunol 2005;15(1):81-3.

See these in context on the Pau D'arco monograph →

Thyme 18 references
  1. Zava DT, Dollbaum CM, Blen M. Estrogen and progestin bioactivity of foods, herbs, and spices. Proc Soc Exp Biol Med 1998;217:369-78. PubMed
  2. Electronic Code of Federal Regulations. Title 21. Part 182 -- Substances Generally Recognized As Safe. Available at: https://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfcfr/CFRSearch.cfm?CFRPart=182
  3. Okazaki K, Kawazoe K, Takaishi Y. Human platelet aggregation inhibitors from thyme (Thymus vulgaris L.). Phytother Res 2002;16:398-9. .
  4. Spiewak R, Skorska C, Dutkiewicz J. Occupational airborne contact dermatitis caused by thyme dust. Contact Dermatitis 2001;44:235-9. . PubMed
  5. Ernst E, Marz R, Sieder C. A controlled multi-centre study of herbal versus synthetic secretolytic drugs for acute bronchitis. Phytomedicine 1997;4:287-93. PubMed
  6. Yamamoto J, Yamada K, Naemura A, et al. Testing various herbs for antithrombotic effect. Nutrition 2005;21(5):580-7. PubMed
  7. Tognolini, M., Barocelli, E., Ballabeni, V., Bruni, R., Bianchi, A., Chiavarini, M., and Impicciatore, M. Comparative screening of plant essential oils: phenylpropanoid moiety as basic core for antiplatelet activity. Life Sci. 2-23-2006;78(13):1419-1432. PubMed
  8. Mackiewicz, B., Skorska, C., Dutkiewicz, J., Michnar, M., Milanowski, J., Prazmo, Z., Krysinska-Traczyk, E., and Cisak, E. Allergic alveolitis due to herb dust exposure. Ann Agric Environ Med 1999;6(2):167-170.
  9. Martinez-Gonzalez, M. C., Goday Bujan, J. J., Martinez, Gomez W., and Fonseca, Capdevila E. Concomitant allergic contact dermatitis due to Rosmarinus officinalis (rosemary) and Thymus vulgaris (thyme). Contact Dermatitis 2007;56(1):49-50.
  10. Jukic, M., Politeo, O., Maksimovic, M., Milos, M., and Milos, M. In vitro acetylcholinesterase inhibitory properties of thymol, carvacrol and their derivatives thymoquinone and thymohydroquinone. Phytother.Res 2007;21(3):259-261.
  11. Marzian, O. [Treatment of acute bronchitis in children and adolescents. Non-interventional postmarketing surveillance study confirms the benefit and safety of a syrup made of extracts from thyme and ivy leaves]. MMW.Fortschr.Med 6-28-2007;149(27-28 Suppl
  12. Cuzzolin, L. and Benoni, G. Attitudes and knowledge toward natural products safety in the pharmacy setting: an Italian study. Phytother.Res 2009;23(7):1018-1023. PubMed
  13. Berova, N., Stransky, L., and Krasteva, M. Studies on contact dermatitis in stomatological staff. Dermatol.Monatsschr. 1990;176(1):15-18.
  14. Smeenk, G., Kerckhoffs, H. P., and Schreurs, P. H. Contact allergy to a reaction product in Hirudoid cream: an example of compound allergy. Br.J Dermatol. 1987;116(2):223-231.
  15. Le Roy, R., Grosshans, E., and Foussereau, J. [Investigation of contact allergies in 100 cases of ulcus cruris (author's transl)]. Derm.Beruf.Umwelt. 1981;29(6):168-170.
  16. Lorenzi, S., Placucci, F., Vincenzi, C., Bardazzi, F., and Tosti, A. Allergic contact dermatitis due to thymol. Contact Dermatitis 1995;33(6):439-440. PubMed
  17. Bahadoran P, Rokni FK, Fahami F. Investigating the therapeutic effect of vaginal cream containing garlic and thyme compared to clotrimazole cream for the treatment of mycotic vaginitis. Iran J Nurs Midwifery Res 2010;15(Suppl 1):343-9.
  18. Erol S, Aydin B, Dilli D, Okumus N, Zenciroglu A, Gündüz M. An interesting newborn case of fructose 1-6 diphosphatase deficiency triggered after thyme juice ingestion. Clin Lab. 2014;60(1):151-3. PubMed

See these in context on the Thyme monograph →

Echinacea 51 references
  1. Mullins RJ. Echinacea-associated anaphylaxis. Med J Aust 1998;168:170-1. PubMed
  2. Mullins RJ. Allergic reactions to Echinacea. J Allergy Clin Immunol 2000;104:S340-341 (Abstract 1003).
  3. Chavez ML, Chavez PI. Echinacea. Hosp Pharm 1998;33:180-8.
  4. Grimm W, Muller HH. A randomized controlled trial of the effect of fluid extract of Echinacea purpurea on the incidence and severity of colds and respiratory infections. Am J Med 1999;106:138-43. PubMed
  5. Taylor JA, Weber W, Standish L, et al. Efficacy and safety of echinacea in treating upper respiratory tract infections in children: a randomized controlled trial. JAMA 2003;290:2824-30.. PubMed
  6. Luettig B, Steinmuller C, Gifford GE, et al. Macrophage activation by the polysaccharide arabinogalactan isolated from plant cell cultures of Echinacea purpurea. J Natl Cancer Inst 1989;81:669-75. PubMed
  7. Stimpel M, Proksch A, Wagner H, et al. Macrophage activation and induction of macrophage cytotoxicity by purified polysaccharide fractions from the plant Echinacea purpurea. Infect Immun 1984;46:845-9. PubMed
  8. Budzinski JW, Foster BC, Vandenhoek S, Arnason JT. An in vitro evaluation of human cytochrome P450 3A4 inhibition by selected commercial herbal extracts and tinctures. Phytomedicine 2000;7:273-82. PubMed
  9. Gallo M, Sarkar M, Au W, et al. Pregnancy outcome following gestational exposure to echinacea: A prospective controlled study. Arch Intern Med 2000;160:3141-3. PubMed
  10. Soon SL, Crawford RI. Recurrent erythema nodosum associated with echinacea herbal therapy. J Am Acad Dermatol 2001;44:298-9. PubMed
  11. Mullins RJ, Heddle R. Adverse reactions associated with echinacea: the Australian experience. Ann Allergy Asthma Immunol 2002;88:42-51. PubMed
  12. Logan JL, Ahmed J. Critical hypokalemic renal tubular acidosis due to Sjogren's syndrome: association with the purported immune stimulant echinacea. Clin Rheumatol 2003;22:158-9.
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See these in context on the Echinacea monograph →

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See these in context on the Ginkgo monograph →

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

© 2021 Therapeutic Research Center, LLC

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