Major interaction on record — check this product against your medications before combining. Based on 17 of 18 ingredients. Check your meds →
Dietary supplement

Rize 2 The Occasion Ingredients & Drug Interactions

by We Care Distributor

Rize 2 The Occasion label
See full label image
Capsule Category: Other Combinations
Most serious interaction: Major
Clinical methodology reviewed by · Updated Sep 16, 2026 · Label data from the NIH DSLD
What is this page for?

First and foremost: checking Rize 2 The Occasion against your medications. The heart of this page is the interaction checker and the full interaction report — how this product’s ingredients may interact with prescription and over-the-counter medicines you may be taking.

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

The interaction bottom line Most serious interaction: Major

Rize 2 The Occasion is a dietary supplement by We Care Distributor with 18 active ingredients. Its ingredients are commonly taken for erectile dysfunction, low sex drive, sexual performance.Based on those ingredients, 1,727 medications have a known interaction with it, the most serious rated major. The ingredients most likely to interact are Ginkgo biloba extract, Panax ginseng root extract, Yohimbine HCl. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.

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Check Your Meds Against Rize 2 The Occasion by We Care Distributor

Ask about any prescription or over-the-counter medication and we check it for interactions with Rize 2 The Occasion by We Care Distributor — and tell you which ingredient is responsible.

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Computed from our clinical databases

HelloPharmacist Scorecard of Rize 2 The Occasion by We Care Distributor

Four independent checks of what is known — a summary of the available information, not a grade of the product itself.

Evidence for Intended Use
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 assessable

The stated purpose hasn't been mapped to our evidence data yet.

Why this rating?
  • We haven't mapped this product's purpose to our evidence data yet — it'll be graded on the next content refresh.
Ingredient Transparency
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 6 of its 18 active ingredients.
  • “Proprietary Blend” is a proprietary blend — the label gives one combined amount (440 mg) without saying how much of each component you get.
Known Interaction Concern
Major identified

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

Why this rating?
  • 14 of the 17 matched ingredients can interact with medications — Tribulus, Ginkgo, Cordyceps, Horny Goat Weed, Yohimbe, among others.
  • 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; lithium; Parkinson's medications.
  • For scale: 1,728 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.
Safety Information
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 15 of the 17 matched ingredients.
  • Pregnancy & breastfeeding safety ratings cover 17 of 17.
  • General safety write-ups exist for 17 of 17.
  • Remember: this measures how much safety information exists. Thin data is not the same as being safe.

HelloPharmacist summaryFormula with limited ingredient disclosure with no assessable stated purpose. Major medication interactions have been identified, and safety information is well characterized.

Assessment coverage: 17 of 18 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated Dec 18, 2021.

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 Rize 2 The Occasion, straight from the product label.

Brand We Care Distributor
Barcode (UPC) 370005112016
Net contents 1 Capsule(s)
Market status Off market
Date entered into DSLD Dec 18, 2021
DSLD ID 264472
Product type Other Combinations
Supplement form Capsule
Dietary claims / uses All Other, Structure/Function
Intended target group(s) Women (not pregnant or lactating), 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 Rize 2 The Occasion by We Care Distributor, 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:
1 Capsule(s)
UPC/BARCODE
370005112016
IngredientAmount% DV
Proprietary Blend440 mg--
Yohimbine HCl0 NP--
Vitamin B330 mg150%
Maca Root Extract60 mg--
Panax ginseng root extract0 NP--
Saw Palmetto extract0 NP--
Ginkgo biloba extract0 NP--
Piper nigrum extract5 mg--
Tongkat Ali Extract40 mg--
Mucuna pruriens0 NP--
L-Arginine HCl0 NP--
Boron2.5 mg--
Tribulus terrestris extract0 NP--
Muira Puama Extract0 NP--
Butea superba Extract0 NP--
Horny Goat Weed Leaf Extract90 mg--
Cordyceps0 NP--
Momordica charantia Extract0 NP--
Xian Mao Extract0 NP--

Other ingredients: Maltodextrin, Silicon Dioxide, Magnesium Stearate, Gelatin, Titanium Dioxide, FD&C Red #40

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.
Formulation

Sexual performance Enhancer

The ultimate sexual performance enhancer

Formula

For men

FDA Statement of Identity

Dietary Supplement

Precautions

Must be at least 18 years of age to use this product

Warning: Keep out of reach of children. Not intended for persons under the age of 18.

Use only as directed. Do not exceed recommended dosage. Do not use if tamper-resistant seal is broken or missing.

Do not use if pregnant, nursing, taking MAOI's or anti-depressants, or if you are at risk of or are being treated for high blood pressure, heart or prostate conditions, kidney disease or any other pre-existing medical condition.

Always consult with a licensed physician orpharmacist prior to taking this, or any, dietary supplement. Discontinue use immediately and consult a doctor if you have and adverse reaction to this product.

Seals/Symbols

GMP Good Manufacturing Practice Consistent Quality Made in USA

Suggested/Recommended/Usage/Directions

Suggested Use: As a dietary supplement, take 1 capsule with plenty of water one hour prior to sexual performance as needed, or as directed by your healthcare practitioner.

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.

Storage

Store at room temperature in a cool,dry

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

See for yourself

Rize 2 The Occasion by We Care Distributor label

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

Rize 2 The Occasion label

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

View the full label (PDF)
What’s inside

The Ingredients in Rize 2 The Occasion by We Care Distributor

These are the 18 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.

Vitamin B3

Interacts with
727 drugs
30 mg per serving Form: Niacin

Niacin (vitamin B3) is an essential nutrient your body needs for energy and metabolism, and deficiency is uncommon in most developed countries. Prescr...

Vitamin B3 monograph & interactions

Maca Root Extract

No known
interactions
60 mg per serving

Maca is a nutrient-rich Andean root often used for energy, libido, and menopause symptoms. Early studies suggest it may modestly help sexual desire an...

Maca Root Extract monograph & interactions

Piper nigrum extract

Interacts with
1,019 drugs
5 mg per serving

Black pepper is a common kitchen spice that is generally safe in the amounts used in food. Its extract, piperine, is mostly added to supplements to he...

Piper nigrum extract monograph & interactions

Tongkat Ali Extract

Interacts with
248 drugs
40 mg per serving

Eurycoma longifolia (tongkat ali) is a Southeast Asian herb most popular for supporting testosterone, libido, and male fertility, with some small huma...

Tongkat Ali Extract monograph & interactions

Boron

No known
interactions
2.5 mg per serving Form: Boron Citrate

Boron is a trace mineral found in many plant foods and sold as a supplement, mainly promoted for bone, joint, and hormone health. The human evidence f...

Boron monograph & interactions

Horny Goat Weed Leaf Extract

Interacts with
963 drugs
90 mg per serving

Horny goat weed (Epimedium) is a traditional Chinese herb most often marketed for low libido and erectile problems, but solid human evidence for these...

Horny Goat Weed Leaf Extract monograph & interactions

Other (inactive) ingredients: Maltodextrin, Silicon Dioxide, Magnesium Stearate, Gelatin, Titanium Dioxide, FD&C Red #40. These complete the product’s ingredient list but are not active constituents.

Interaction report

Rize 2 The Occasion by We Care Distributor Drug Interactions

Rize 2 The Occasion contains 18 ingredients, and 14 of them have known drug interactions. Altogether they interact with 1,727 medications. Here’s the picture, then you can look up your own drug.

Want to check YOUR meds against Rize 2 The Occasion?

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
1,727Drugs
18 Major 1,709 Moderate

Ingredients driving the most interactions

Ginkgo biloba extract 1,266
Panax ginseng root extract 1,130
Yohimbine HCl 1,125
Piper nigrum extract 1,019
Horny Goat Weed Leaf Extract 963

Individual Drug Interactions

The ingredients in Rize 2 The Occasion interact with 1,727 drugs. Click any drug to see the details.

14 of the 18 ingredients in Rize 2 The Occasion interact with drugs. Each result below shows which ingredient is responsible. Ginkgo biloba extract Panax ginseng root extract Yohimbine HCl Piper nigrum extract Horny Goat Weed Leaf Extract Vitamin B3 L-Arginine HCl Momordica charantia Extract Tribulus terrestris extract Cordyceps Tongkat Ali Extract Mucuna pruriens Saw Palmetto extract Butea superba Extract

Each ingredient & the kinds of drugs it affects

For each ingredient in Rize 2 The Occasion 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.

Ginkgo biloba extract23 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
Ginkgo biloba extract full monograph & interactions

Panax ginseng root extract20 drug types · 1,130 drugs

Anticoagulant/Antiplatelet Drugs

Although Panax ginseng has shown antiplatelet effects in the laboratory, it is unlikely to increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
In vitro evidence suggests that ginsenoside constituents in Panax ginseng might decrease platelet aggregation. However, research in humans suggests that ginseng does not affect platelet aggregation. Animal research indicates low oral bioavailability of Rb1 and rapid elimination of Rg1, which might explain the discrepancy between in vitro and human research. Until more is known, use with caution in patients concurrently taking anticoagulant or antiplatelet drugs.

Likelihood Unlikely Evidence B
Antidiabetes Drugs

Theoretically, taking Panax ginseng with antidiabetes drugs might increase the risk of hypoglycemia.
Clinical research suggests that Panax ginseng might decrease blood glucose levels. Monitor blood glucose levels closely.

Likelihood Probable Evidence B
Caffeine

Theoretically, taking Panax ginseng with caffeine might increase the risk of adverse stimulant effects.
Panax ginseng has been shown to have stimulant effects. Theoretically, caffeine might have an additive effect on the stimulant effects of Panax ginseng.

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

Theoretically, Panax ginseng might increase levels of drugs metabolized by CYP2D6. However, research is conflicting.
There is some evidence that Panax ginseng can inhibit the CYP2D6 enzyme by approximately 6%. In addition, in animal research, Panax ginseng inhibits the metabolism of dextromethorphan, a drug metabolized by CYP2D6, by a small amount. However, contradictory research suggests Panax ginseng might not inhibit CYP2D6. Until more is known, use Panax ginseng cautiously in patients taking drugs metabolized by these enzymes.

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

Theoretically, Panax ginseng might increase or decrease levels of drugs metabolized by CYP3A4.
Panax ginseng may affect the clearance of drugs metabolized by CYP3A4. One such drug is imatinib. Inhibition of CYP3A4 was believed to be responsible for a case of imatinib-induced hepatotoxicity. In contrast, Panax ginseng has been shown to increase the clearance of midazolam, another drug metabolized by CYP3A4. Clinical research shows that Panax ginseng can reduce midazolam area under the curve by 44%, maximum plasma concentration by 26%, and time to reach maximum plasma concentration by 29%. Midazolam metabolism was also increased in animals given Panax ginseng. Until more is known, use Panax ginseng cautiously in combination with CYP3A4 substrates.

Likelihood Possible Evidence B
Estrogens

Theoretically, concomitant use of large amounts of Panax ginseng might interfere with hormone replacement therapy.
Laboratory research and some case reports suggest that Panax ginseng can have estrogenic effects due to competition for estrogen receptors. The estrogenic activity is attributed to the ginsenoside constituents of Panax ginseng.

Likelihood Possible Evidence D
Furosemide (Lasix)

Theoretically, Panax ginseng might reduce the effects of furosemide.
There is some concern that Panax ginseng might contribute to furosemide resistance. There is one case of resistance to furosemide diuresis in a patient taking a germanium-containing ginseng product.

Likelihood Possible Evidence D
Imatinib (Gleevec)

Theoretically, Panax ginseng might increase the effects and adverse effects of imatinib.
A case of imatinib-induced hepatotoxicity has been reported for a 26-year-old male with chronic myelogenous leukemia stabilized on imatinib for 7 years. The patient took imatinib 400 mg along with a Panax ginseng-containing energy drink daily for 3 months. Since imatinib-associated hepatotoxicity typically occurs within 2 years of initiating therapy, it is believed that Panax ginseng affected imatinib toxicity though inhibition of cytochrome P450 3A4. CYP3A4 is the primary enzyme involved in imatinib metabolism.

Likelihood Possible Evidence D
Immunosuppressants

Theoretically, Panax ginseng use might interfere with immunosuppressive therapy.
Panax ginseng might have immune system stimulating properties.

Likelihood Possible Evidence B
Insulin

Theoretically, taking Panax ginseng with insulin might increase the risk of hypoglycemia.
Clinical research suggests that Panax ginseng might decrease blood glucose levels. Insulin dose adjustments might be necessary in patients taking Panax ginseng; use with caution.

Likelihood Probable Evidence B
Midazolam (Versed)

Theoretically, Panax ginseng may increase the clearance of midazolam.
Midazolam is metabolized by cytochrome P450 3A4 (CYP3A4). Clinical research suggests that Panax ginseng can reduce midazolam area under the curve by 44%, maximum plasma concentration by 26%, and time to reach maximum plasma concentration by 29%. Midazolam metabolism was also increased in animals given Panax ginseng.

Likelihood Probable Evidence B
Monoamine Oxidase Inhibitors (Maois)

Theoretically, Panax ginseng can interfere with MAOI therapy.
Concomitant use of Panax ginseng with phenelzine (Nardil) is associated with insomnia, headache, tremors, and hypomania.

Likelihood Probable Evidence D
Nifedipine (Procardia)

Theoretically, taking Panax ginseng with nifedipine might increase serum levels of nifedipine and the risk of hypotension.
Preliminary clinical research shows that concomitant use can increase serum levels of nifedipine in healthy volunteers. This might cause the blood pressure lowering effects of nifedipine to be increased when taken concomitantly with Panax ginseng.

Likelihood Possible Evidence B
Qt Interval-Prolonging Drugs

Theoretically, Panax ginseng has an additive effect with drugs that prolong the QT interval and potentially increase the risk of ventricular arrhythmias. However, research is conflicting.
Clinical research shows that short-term use of Panax ginseng can increase the QT interval. However, no changes in QT interval have been identified with prolonged use.

Likelihood Possible Evidence B
Raltegravir (Isentress)

Theoretically, taking Panax ginseng with raltegravir might increase the risk of liver toxicity.
A case report suggests that concomitant use of Panax ginseng with raltegravir can increase serum levels of raltegravir, resulting in elevated liver enzymes levels.

Likelihood Possible Evidence D
Selegiline (Eldepryl)

Theoretically, Panax ginseng might increase or decrease levels of selegiline, possibly altering the effects and side effects of selegiline.
Animal research shows that taking selegiline with a low dose of Panax ginseng extract (1 gram/kg) reduces selegiline bioavailability, while taking a high dose of Panax ginseng extract (3 grams/kg) increases selegiline bioavailability. More research is needed to confirm these effects.

Likelihood Possible Evidence D
Stimulant Drugs

Theoretically, taking Panax ginseng with stimulant drugs might increase the risk of adverse stimulant effects.
Panax ginseng has been shown to have stimulant effects.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Panax ginseng might affect the clearance of warfarin. However, this interaction appears to be unlikely.
There has been a single case report of decreased effectiveness of warfarin in a patient who also took Panax ginseng. However, it is questionable whether Panax ginseng was the cause of this decrease in warfarin effectiveness. Some research in humans and animals suggests that Panax ginseng does not affect the pharmacokinetics of warfarin. However, other research in humans suggests that Panax ginseng might modestly increase the clearance of the S-warfarin isomer. More evidence is needed to determine whether Panax ginseng causes a significant interaction with warfarin.

Likelihood Unlikely Evidence B
Fexofenadine (Allegra)

Theoretically, Panax ginseng might decrease blood levels of oral or intravenous fexofenadine.
Animal research suggests that taking Panax ginseng in combination with oral or intravenous fexofenadine may reduce the bioavailability of fexofenadine. Some scientists have attributed this effect to the ability of Panax ginseng to increase the expression of P-glycoprotein.

Likelihood Possible Evidence D
Lopinavir/Ritonavir (Kaletra)

Although Panax ginseng has demonstrated variable effects on cytochrome P450 3A4 (CYP3A4), which metabolizes lopinavir, Panax ginseng is unlikely to alter levels of lopinavir/ritonavir.
Lopinavir is metabolized by CYP3A4 and is administered with the CYP3A4 inhibitor ritonavir to increase its plasma concentrations. Panax ginseng has shown variable effects on CYP3A4 activity in humans. However, taking Panax ginseng (Vitamer Laboratories) 500 mg twice daily for 14 days did not alter the pharmacokinetics of lopinavir/ritonavir in 12 healthy volunteers.

Likelihood Unlikely Evidence B
Panax ginseng root extract full monograph & interactions

Yohimbine HCl13 drug types · 1,125 drugs

Monoamine Oxidase Inhibitors (Maois)

Concomitant use of MAOIs with yohimbe can result in additive effects.
Yohimbine, a constituent of yohimbe, has MAO inhibitory effects. At high doses, yohimbine is a non-selective inhibitor of MAO.

Likelihood Likely Evidence D
Antihypertensive Drugs

Theoretically, yohimbe might reduce the effects of antihypertensive drugs.
Yohimbine, a constituent of yohimbe, is an alpha-2 adrenoceptor antagonist and has been reported to increase blood pressure in clinical research. Theoretically, concomitant use of yohimbe and antihypertensive drugs can interfere with blood pressure control.

Likelihood Probable Evidence D
Clonidine (Catapres)

Theoretically, yohimbe might precipitate clonidine withdrawal.
Chronic clonidine use can downregulate alpha-2 adrenoreceptors. Animal research and one human case report suggest that concomitant administration of yohimbine, an alpha-2 adrenoceptor antagonist, may precipitate clonidine withdrawal and lead to sympathomimetic toxicity, including hypertensive crisis.

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

CYP2D6 inhibitors may increase the levels and adverse effects of yohimbine, a constituent of yohimbe.
In vitro and clinical research shows that the yohimbe bark constituent, yohimbine, is metabolized by CYP2D6 isoenzymes. Paroxetine, a cytochrome P450 (CYP) 2D6 inhibitor, increases the maximum serum concentration of yohimbine and reduces the clearance of yohimbine compared to yohimbine alone in patients who are extensive CYP2D6 metabolizers..

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

Theoretically, yohimbe might increase the levels and adverse effects of CYP2D6 substrates.
In vitro research suggests that yohimbine, a constituent of yohimbe bark, inhibits CYP2D6 enzyme activity.

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

Theoretically, CYP3A4 inhibitors might increase the levels and adverse effects of yohimbine, a constituent of yohimbe bark.
In vitro and clinical research shows that the yohimbe bark constituent, yohimbine, is metabolized by CYP3A4 enzymes. Theoretically, drugs that inhibit CYP3A4 might increase the levels and adverse effects of yohimbine.

Likelihood Possible Evidence D
Paroxetine (Paxil)

Paroxetine decreases the clearance of yohimbine and may increase its effects.
Paroxetine, a cytochrome P450 (CYP) 2D6 inhibitor, increases the maximum serum concentration of yohimbine by about 350% and reduces the clearance of yohimbine by about 80% compared to yohimbine alone in patients who are extensive CYP2D6 metabolizers. No significant changes in pharmacokinetic parameters of yohimbine were observed with coadministration of paroxetine in patients who are poor CYP2D6 metabolizers.

Likelihood Probable Evidence B
Phenothiazines

Theoretically, using yohimbine with phenothiazines might have additive effects.
Yohimbine, a constituent of yohimbe, has alpha-2 adrenergic antagonist effects. Theoretically, combining it with phenothiazines can cause additive alpha-2 adrenergic antagonism.

Likelihood Possible Evidence D
Stimulant Drugs

Theoretically, taking yohimbe with stimulant drugs can have additive effects.
Yohimbine, a constituent of yohimbe, has sympathomimetic effects and increases blood pressure in a dose-dependent manner. Theoretically, taking yohimbe with stimulant drugs can have additive stimulant and hypertensive effects.

Likelihood Possible Evidence D
Tricyclic Antidepressants (Tcas)

Theoretically, taking yohimbe with TCAs can increase adverse effects.
A small clinical study in patients taking TCAs for at least 4 weeks shows that receiving doses of intravenous yohimbine 2.5-20 mg daily for up to 7 days precipitates severe anxiety, agitation, and tremor. The effects of yohimbe bark itself are unclear; oral yohimbe bark contains 0.6% to 1.38% yohimbine, but it is unclear how much is absorbed.

Likelihood Possible Evidence D
Anticoagulant/Antiplatelet Drugs

Theoretically, combining yohimbe bark with antiplatelet or anticoagulant drugs might have additive effects; however, this has not been reported in clinical research.
Research in healthy adults shows that taking yohimbine, a constituent of yohimbe bark, in doses of 8 mg or more, seems to inhibit platelet aggregation in vitro by binding to the alpha-2 adrenoceptor. The effects of yohimbe bark itself are unclear; yohimbe bark contains 0.6% to 1.38% yohimbine, but it is unclear how much is absorbed.

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

Theoretically, yohimbe might decrease the levels and clinical effects of CYP1A2 substrates.
In vitro research shows that yohimbe extract induces CYP1A2 enzymes.

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

Theoretically, yohimbe might decrease the levels and clinical effects of CYP3A4 substrates.
In vitro research shows that yohimbe extract induces CYP3A4 enzymes.

Likelihood Possible Evidence D
Yohimbine HCl full monograph & interactions

Piper nigrum extract17 drug types · 1,019 drugs

Anticoagulant/Antiplatelet Drugs

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

Likelihood Possible Evidence D
Antidiabetes Drugs

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

Likelihood Possible Evidence D
Atorvastatin (Lipitor)

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

Likelihood Possible Evidence D
Cyclosporine (Neoral, Sandimmune)

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

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

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

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

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

Likelihood Possible Evidence D
Lithium

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

Likelihood Probable Evidence D
Nevirapine (Viramune)

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

Likelihood Probable Evidence D
P-Glycoprotein Substrates

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

Likelihood Possible Evidence D
Pentobarbital (Nembutal)

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

Likelihood Possible Evidence D
Phenytoin (Dilantin)

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

Likelihood Possible Evidence B
Propranolol (Inderal)

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

Likelihood Possible Evidence B
Rifampin (Rifadin)

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

Likelihood Possible Evidence B
Theophylline

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

Likelihood Possible Evidence D
Amoxicillin (Amoxil, Trimox)

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

Likelihood Possible Evidence D
Carbamazepine (Tegretol)

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

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

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

Likelihood Possible Evidence D
Piper nigrum extract full monograph & interactions

Horny Goat Weed Leaf Extract6 drug types · 963 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, horny goat weed might increase the risk of bleeding.
In vitro research and animal research shows that horny goat weed can inhibit platelet aggregation and thrombus formation. This effect has not been reported in humans.

Likelihood Possible Evidence D
Antihypertensive Drugs

Theoretically, horny goat weed might increase the risk of hypotension.
Laboratory research suggests that horny goat weed might have hypotensive effects. This effect has not been reported in humans.

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

Theoretically, horny goat weed might increase the effects and side effects of CYP1A2 substrates.
In vitro, horny goat weed leaf extract inhibits CYP1A2. This effect has not been reported in humans.

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

Theoretically, horny goat weed might increase the effects and side effects of CYP2B6 substrates.
In vitro, horny goat weed leaf extract inhibits CYP2B6. This effect has not been reported in humans.

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

Theoretically, horny goat weed might increase the effects and side effects of CYP3A4 substrates.
In vitro, horny goat weed extract inhibits CYP3A4 and suppresses CYP3A4 mRNA expression. This effect has not been reported in humans.

Likelihood Possible Evidence D
Estrogens

Theoretically, concomitant use of horny goat weed with estrogens might increase their therapeutic and adverse effects.
In vitro evidence suggests that horny goat weed has estrogenic activity. In clinical research, horny goat weed has been shown to increase blood levels of estrogen in some females.

Likelihood Possible Evidence D
Horny Goat Weed Leaf Extract full monograph & interactions

Vitamin B315 drug types · 727 drugs

Alcohol (Ethanol)

Concomitant use of alcohol and niacin might increase the risk of flushing and hepatotoxicity.
Alcohol can exacerbate the flushing and pruritus associated with niacin. Large doses of niacin might also exacerbate liver dysfunction associated with chronic alcohol use. A case report describes delirium and lactic acidosis in a patient taking niacin 3 grams daily who ingested 1 liter of wine. Advise patients to avoid large amounts of alcohol while taking niacin.

Likelihood Probable Evidence D
Allopurinol (Zyloprim)

Theoretically, niacin might antagonize the therapeutic effects of uricosurics such as allopurinol.
Large doses of niacin can reduce urinary excretion of uric acid, potentially resulting in hyperuricemia. Doses of uricosurics such as allopurinol might need to be increased to maintain control of gout in patients who start taking niacin. People who have frequent attacks of gout despite uricosuric therapy should avoid niacin.

Likelihood Probable Evidence C
Anticoagulant/Antiplatelet Drugs

Theoretically, niacin may have additive effects when used with anticoagulant or antiplatelet drugs.
Several cases of clotting factor synthesis deficiency and coagulopathy have been reported in patients taking sustained-release niacin. Also, thrombocytopenia has been reported in patients treated with niacin or niacin plus lovastatin.

Likelihood Possible Evidence D
Antidiabetes Drugs

Niacin can increase blood glucose levels and may diminish the effects of antidiabetes drugs.
Niacin impairs glucose tolerance in a dose-dependent manner, probably by causing or aggravating insulin resistance and increasing hepatic production of glucose. In diabetes patients, niacin 4.5 grams daily for 5 weeks can increase plasma glucose by an average of 16% and glycated hemoglobin (HbA1c) by 21%. However, lower doses of 1.5 grams daily or less appear to have minimal effects on blood glucose. In some patients, glucose levels increase when niacin is started, but then return to baseline when a stable dose is reached. Up to 35% of patients with diabetes may need adjustments in hypoglycemic therapy when niacin is added.

Likelihood Probable Evidence B
Antihypertensive Drugs

Theoretically, niacin may increase the risk of hypotension when used with antihypertensive drugs.
The vasodilating effects of niacin can cause hypotension. Furthermore, some clinical evidence suggests that a one-hour infusion of niacin can reduce systolic, diastolic, and mean blood pressure in hypertensive patients. This effect is not observed in normotensive patients.

Likelihood Possible Evidence B
Bile Acid Sequestrants

Bile acid sequestrants can bind niacin and decrease absorption. Separate administration by 4-6 hours to avoid an interaction.
In vitro studies show that colestipol (Colestid) binds about 98% of available niacin and cholestyramine (Questran) binds 10% to 30%.

Likelihood Possible Evidence D
Gemfibrozil (Lopid)

Theoretically, concomitant use of niacin and gemfibrozil might increase the risk of myopathy in some patients.
A case of myopathy from concomitant use of niacin and gemfibrozil has been reported. Niacin alone has also been associated with cases of myopathy. Using gemfibrozil with niacin might further increase the risk of developing myopathy.

Likelihood Possible Evidence D
Hepatotoxic Drugs

Theoretically, concomitant use of niacin and hepatotoxic drugs might increase the risk of hepatotoxicity.
Niacin has been associated with cases of liver toxicity, especially when used in pharmacologic doses. Sustained-release niacin preparations appear to be associated with a higher risk of hepatotoxicity than immediate-release niacin.

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

Theoretically, concomitant use of niacin and statins might increase the risk of myopathy and rhabdomyolysis in some patients.
Some case reports have raised concerns that niacin might increase the risk of myopathy and rhabdomyolysis when combined with statins. However, a significantly increased risk of myopathy has not been demonstrated in clinical trials, including those using an FDA-approved combination of lovastatin and niacin (Advicor).

Likelihood Possible Evidence D
Probenecid (Benemid)

Theoretically, niacin might antagonize the therapeutic effects of uricosurics such as probenecid.
Large doses of niacin reduce urinary excretion of uric acid, potentially causing hyperuricemia. Doses of uricosurics such as probenecid might need to be increased to maintain control of gout in patients who start taking niacin. People who have frequent attacks of gout despite uricosuric therapy should avoid niacin.

Likelihood Probable Evidence C
Sulfinpyrazone (Anturane)

Theoretically, niacin might antagonize the therapeutic effects of uricosurics such as sulfinpyrazone.
Large doses of niacin reduce urinary excretion of uric acid, potentially causing hyperuricemia. Doses of uricosurics such as sulfinpyrazone might need to be increased to maintain control of gout in patients who start taking niacin. People who have frequent attacks of gout despite uricosuric therapy should avoid niacin.

Likelihood Probable Evidence C
Thyroid Hormone

Theoretically, niacin might antagonize the therapeutic effects of thyroid hormones.
Clinical research and case reports suggests that taking niacin can reduce serum levels of thyroxine-binding globulin by up to 25% and moderately reduce levels of thyroxine (T4). Patients taking thyroid hormone for hypothyroidism might need dose adjustments when using niacin.

Likelihood Probable Evidence D
Transdermal Nicotine (Nicoderm)

Theoretically, concomitant use of niacin and transdermal nicotine might increase the risk of flushing and dizziness.
Niacin and nicotine can both cause flushing and dizziness.

Likelihood Possible Evidence D
Warfarin (Coumadin)

There is limited evidence that niacin may increase the anticoagulant effects of warfarin.
In a case report, a patient on warfarin developed an elevated international normalized ratio (INR) of 3.9 after taking niacin for two weeks. The patient's INR was previously stable, ranging between 2 and 3 in recent months, and no other medication changes were identified. The elevated INR returned to therapeutic range within 4 days following the discontinuation of niacin.

Likelihood Possible Evidence D
Aspirin

Large doses of aspirin might alter the clearance of niacin.
Aspirin is often used with niacin to reduce niacin-induced flushing. Doses of 80-975 mg aspirin have been used, but 325 mg appears to be optimal. Aspirin also seems to reduce the clearance of niacin by competing for glycine conjugation. Taking aspirin 1 gram seems to reduce niacin clearance by 45%. This is probably a dose-related effect and not clinically significant with the more common aspirin dose of 325 mg.

Likelihood Likely Evidence B
Vitamin B3 full monograph & interactions

L-Arginine HCl9 drug types · 403 drugs

Ace Inhibitors (Aceis)

Theoretically, concomitant use of L-arginine and ACE inhibitors may increase the risk for hypotension and hyperkalemia.
Combining L-arginine with some antihypertensive drugs, especially ACE inhibitors, seems to have additive vasodilating and blood pressure-lowering effects. Furthermore, ACE inhibitors can increase potassium levels. Use of L-arginine has been associated with hyperkalemia in some patients. Theoretically, concomitant use of ACE inhibitors with L-arginine may increases the risk of hyperkalemia.

Likelihood Probable Evidence D
Angiotensin Receptor Blockers (Arbs)

Theoretically, concomitant use of L-arginine and ARBs may increase the risk of hypotension and hyperkalemia.
L-arginine increases nitric oxide, which causes vasodilation. Combining L-arginine with ARBs seems to increase L-arginine-induced vasodilation. Furthermore, ARBs can increase potassium levels. Use of L-arginine has been associated with hyperkalemia in some patients. Theoretically, concomitant use of ARBs with L-arginine may increases the risk of hyperkalemia.

Likelihood Probable Evidence D
Anticoagulant/Antiplatelet Drugs

Theoretically, concomitant use of L-arginine with anticoagulant and antiplatelet drugs might have additive effects and increase the risk of bleeding.
Preliminary research suggests that L-arginine infusions reduce platelet aggregation in humans. The clinical significance of this effect is unclear.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, concomitant use of L-arginine might have additive effects with antidiabetes drugs.
Preliminary clinical research shows that L-arginine decreases blood glucose levels in patients with type 2 diabetes.

Likelihood Possible Evidence D
Antihypertensive Drugs

Theoretically, concomitant use of L-arginine and antihypertensive drugs may increase the risk of hypotension.
L-arginine increases nitric oxide, which causes vasodilation. Clinical evidence shows that L-arginine can reduce blood pressure in some individuals with hypertension. Furthermore, combining L-arginine with some antihypertensive drugs seems to have additive vasodilating and blood pressure-lowering effects.

Likelihood Probable Evidence D
Isoproterenol (Isuprel)

Theoretically, concurrent use of isoproterenol and L-arginine might result in additive effects and hypotension.
Preliminary clinical evidence suggests that L-arginine enhances isoproterenol-induced vasodilation in patients with essential hypertension or a family history of essential hypertension.

Likelihood Probable Evidence D
Potassium-Sparing Diuretics

Theoretically concomitant use of potassium-sparing diuretics with L-arginine may increases the risk of hyperkalemia.
Potassium-sparing diuretics can increase potassium levels. Use of L-arginine has been associated with hyperkalemia in some patients.

Likelihood Possible Evidence D
Sildenafil (Viagra)

Theoretically, concurrent use of sildenafil and L-arginine might increase the risk for hypotension.
In vivo, concurrent use of L-arginine and sildenafil has resulted in increased vasodilation. Theoretically, concurrent use might have additive vasodilatory and hypotensive effects. However, in studies evaluating the combined use of L-arginine and sildenafil for erectile dysfunction, hypotension was not reported.

Likelihood Possible Evidence D
Testosterone

Theoretically, concomitant use of L-arginine and testosterone might have additive effects.
In clinical research, L-arginine increases the level of testosterone in male patients with erectile dysfunction. The clinical significance of this finding is unclear.

Likelihood Possible Evidence D
L-Arginine HCl full monograph & interactions

Momordica charantia Extract3 drug types · 282 drugs

Antidiabetes Drugs

Taking bitter melon with antidiabetes drugs might increase the risk of hypoglycemia.
Bitter melon can lower blood glucose levels and might have additive effects when used with antidiabetes drugs. This might increase the risk of hypoglycemia in some patients. Monitor blood glucose levels closely.

Likelihood Probable Evidence B
P-Glycoprotein Substrates

Theoretically, bitter melon might increase levels of P-glycoprotein substrates.
Bitter melon might inhibit the p-glycoprotein (P-gp) intestinal pump and increase intracellular levels of P-gp substrates. In vitro research in intestinal cells shows that 1-monopalmitin, a constituent of bitter melon, increases levels of daunomycin, a P-gp substrate. Additionally, drinking bitter melon juice has been associated with a case of acute pancreatitis in a patient who had been taking pazopanib, a P-gp substrate, for 8 years. Researchers theorize that inhibition of P-gp led to increased levels of pazopanib, resulting in pazopanib-induced pancreatitis.

Likelihood Possible Evidence D
Pazopanib (Votrient)

Theoretically, bitter melon might increase levels of pazopanib, potentially increasing the risk of adverse effects.
In one case, a 65-year-old patient taking pazopanib for 8 years for renal cell carcinoma experienced signs and symptoms consistent with acute pancreatitis 4 days after drinking bitter melon juice at a dose of 100-150 mL daily. The patient's symptoms, amylase levels, and lipase levels improved upon discontinuation of bitter melon and pazopanib. Pazopanib treatment was re-initiated with no further evidence of pancreatitis. Researchers theorize that inhibition of P-glycoprotein by bitter melon led to increased levels of pazopanib, a P-glycoprotein substrate, resulting in pazopanib-induced pancreatitis.

Likelihood Possible Evidence D
Momordica charantia Extract full monograph & interactions

Tribulus terrestris extract3 drug types · 259 drugs

Antidiabetes Drugs

Taking tribulus with antidiabetes drugs might increase the risk of hypoglycemia.
Clinical research shows that Tribulus can lower blood glucose levels in adults with type 2 diabetes who are taking antidiabetes medications.

Likelihood Possible Evidence D
Antihypertensive Drugs

Theoretically, taking tribulus with antihypertensive drugs might increase the risk of hypotension.
Animal research shows that tribulus can lower blood pressure by inhibiting angiotensin-converting enzyme (ACE). Tribulus has also demonstrated hypotensive effects in pre-hypertensive adults.

Likelihood Possible Evidence D
Lithium

Theoretically, tribulus might increase the levels and clinical effects of lithium.
Tribulus is thought to have diuretic properties. Due to these potential diuretic effects, tribulus might reduce excretion and increase levels of lithium. The dose of lithium might need to be decreased.

Likelihood Probable Evidence D
Tribulus terrestris extract full monograph & interactions

Cordyceps3 drug types · 249 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, cordyceps may increase the risk of bleeding when used with antiplatelet or anticoagulant drugs.
In vitro and animal research suggests that cordyceps extract inhibits platelet aggregation and function. However, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Immunosuppressants

Theoretically, concurrent use of cordyceps might interfere with immunosuppressive therapy.
Animal and in vitro research suggests that cordyceps stimulates the immune system. However, limited clinical research suggests that taking cordyceps may lower the necessary therapeutic dose of the immunosuppressant cyclosporine, which suggests that cordyceps may have an immunosuppressive effect.

Likelihood Possible Evidence B
Testosterone

Theoretically, concurrent use of cordyceps and testosterone might have additive effects.
Animal research suggests that cordyceps can increase testosterone levels. The clinical significance of this finding is unclear.

Likelihood Possible Evidence D
Cordyceps full monograph & interactions

Tongkat Ali Extract5 drug types · 248 drugs

Propranolol (Inderal)

Eurycoma longifolia can reduce the levels and clinical effects of propranolol.
A small clinical study in healthy persons shows that taking a single dose of a water-based Eurycoma longifolia extract 200 mg, in combination with a single dose of propranolol 80 mg, reduces the propranolol area under the curve (AUC) by 29%, reduces the peak concentration by 42%, and increases time to peak concentration by 86% when compared with control. Since the elimination half-life of propranolol did not change, it seems that Eurycoma longifolia alters the kinetics of propranolol by decreasing its absorption in the gut, and not by altering its metabolism. It is not known if separating administration will prevent this interaction.

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

Theoretically, Eurycoma longifolia might increase levels CYP1A2 substrates.
In vitro research suggests that methanolic Eurycoma longifolia root extract weakly inhibits CYP1A2 enzymes. This effect has not been reported in humans.

Likelihood Possible Evidence D
Cytochrome P450 2A6 (Cyp2A6) Substrates

Theoretically, Eurycoma longifolia might increase levels of CYP2A6 substrates.
In vitro research suggests that methanolic Eurycoma longifolia root extract weakly inhibits CYP2A6 enzymes. This effect has not been reported in humans.

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

Theoretically, Eurycoma longifolia might increase levels of CYP2C19 substrates.
In vitro research suggests that methanolic Eurycoma longifolia root extract weakly inhibits CYP2C19 enzymes. This effect has not been reported in humans.

Likelihood Possible Evidence D
Testosterone

Theoretically, Eurycoma longifolia may further increase levels of testosterone.
A clinical study in aging males with testosterone levels below 300 ng/dL shows that taking a specific water extract of Eurycoma longifolia roots (Physta; Biotropics Malaysia) 100-200 mg daily with breakfast for 12 weeks increases total testosterone levels by 8% to 11% when compared with placebo. It is unclear whether this increase would occur in individuals with normal testosterone levels.

Likelihood Possible Evidence D
Tongkat Ali Extract full monograph & interactions

Mucuna pruriens8 drug types · 193 drugs

Levodopa

Concomitant use can increase the risk of levodopa-related adverse effects.
Cowhage contains levodopa. Some cowhage products have been standardized to contain 75-400 mg of levodopa per dose.

Likelihood Likely Evidence D
Methyldopa (Aldomet)

Theoretically, concomitant use of cowhage and methyldopa might increase the risk of hypotension.
Cowhage contains levodopa. Use of levodopa with methyldopa might cause additive hypotension. In addition, methyldopa may inhibit peripheral decarboxylation of levodopa and increase levodopa levels in the central nervous system; avoid using.

Likelihood Probable Evidence D
Monoamine Oxidase Inhibitors (Maois)

Theoretically, concomitant use of cowhage and non-selective MAOIs might increase the risk of hypertensive crisis.
Cowhage contains levodopa. Use of levodopa with non-selective MAOIs might cause hypertensive crisis. However, this interaction has not been reported with MAO-B selective inhibitors such as selegiline.

Likelihood Probable Evidence D
Anesthesia

Theoretically, concomitant use of cowhage and anesthesia might increase the risk of arrhythmias.
Cowhage contains levodopa. Use of levodopa with cyclopropane or halogenated hydrocarbon anesthesia has led to arrhythmias. Other anesthetics have not been implicated. Use other anesthetics in patients taking cowhage or tell patients to stop taking cowhage at least 2 weeks before surgery.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, concomitant use of cowhage and antidiabetes drugs might increase the risk of hypoglycemia.
Animal research shows that cowhage might have hypoglycemic effects.

Likelihood Possible Evidence D
Antipsychotic Drugs

Theoretically, use of cowhage might decrease the clinical effects of antipsychotic drugs.
Cowhage contains levodopa. Use of levodopa might counteract the antidopaminergic effects of antipsychotic medications.

Likelihood Possible Evidence D
Guanethidine (Ismelin)

Theoretically, concomitant use of cowhage and guanethidine might increase the risk of hypotension.
Cowhage contains levodopa. Use of levodopa with guanethidine might cause additive hypotension; avoid using.

Likelihood Probable Evidence D
Tricyclic Antidepressants (Tcas)

Theoretically, use of TCAs might reduce the levels and clinical effects of cowhage.
Cowhage contains levodopa. Use of TCAs might reduce the absorption of levodopa. Some case reports describe patients that developed hypertension and dyskinesia when taking both levodopa and TCAs.

Likelihood Possible Evidence D
Mucuna pruriens full monograph & interactions

Saw Palmetto extract3 drug types · 174 drugs

Anticoagulant/Antiplatelet Drugs

Saw palmetto might increase the risk of bleeding with anticoagulant or antiplatelet drugs.
Saw palmetto is reported to prolong bleeding time. Theoretically, it might increase the risk of bleeding when used concomitantly with anticoagulant or antiplatelet drugs.

Likelihood Possible Evidence D
Contraceptive Drugs

Saw palmetto might reduce the effectiveness of contraceptive drugs.
Saw palmetto might have antiestrogenic effects. Theoretically, it might interfere with contraceptive drugs taken concomitantly.

Likelihood Possible Evidence B
Estrogens

Saw palmetto might reduce the effectiveness of estrogens.
Saw palmetto might have antiestrogenic effects. Theoretically, it might interfere with estrogens taken concomitantly.

Likelihood Possible Evidence B
Saw Palmetto extract full monograph & interactions

Butea superba Extract1 drug type · 7 drugs

Phosphodiesterase-5 Inhibitors

Butea superba is thought to inhibit phosphodiesterase and cause vasodilation. Theoretically, concurrent use of phosphodiesterase-5 inhibitors and Butea superba might result in additive vasodilation and hypotension. Phosphodiesterase-5 inhibitors include sildenafil (Viagra), tadalafil (Cialis), and vardenafil (Levitra).

Likelihood Possible Evidence D
Butea superba Extract full monograph & interactions
The maker

Brand information

Manufacturer and brand details for Rize 2 The Occasion, from the product label.

We Care Distributor

See all We Care Distributor products
Name
Amazing 4
Street Address
6965 Plazza Grand Ave Suite #317
City
Orlando
State
FL
ZipCode
32835
Web Address
www.Rize2occasion.com
Pharmacist Counseling Corner

Rize 2 The Occasion by We Care Distributor: Common Questions

Does Rize 2 The Occasion by We Care Distributor interact with any medications?
Yes. Based on its ingredients, Rize 2 The Occasion has a known interaction with 1,727 medications, including 18 rated major. Use the checker to see how it interacts with a specific drug.
How can one product interact with so many drugs?
Rize 2 The Occasion contains 18 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.

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

Not sure if Rize 2 The Occasion is safe with your meds?

Our pharmacists answer your medication & supplement questions — free.

Ask a pharmacist

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.

Rize 2 The Occasion label
Go deeper

The Full Monographs Behind Rize 2 The Occasion’s Ingredients

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

Herb & supplement monograph

Yohimbe

Interacts with 1,125 drugs

Yohimbe is a West African tree bark that contains yohimbine, a compound mainly promoted for erectile dysfunction and as an aphrodisiac. A prescription form of yohimbine has some evidence for...

Read the full Yohimbe monograph → Herb & supplement monograph

Panax Ginseng

Interacts with 1,130 drugs

Panax ginseng is a popular traditional herb used to boost energy, ease stress, and support overall wellness, though scientific evidence is mixed and mostly preliminary. It is generally well...

Read the full Panax Ginseng monograph → Herb & supplement monograph

Saw Palmetto

Interacts with 174 drugs

Saw palmetto is a plant extract most often used for urinary symptoms linked to an enlarged prostate (BPH). The best research suggests it works no better than a placebo for most men, though i...

Read the full Saw Palmetto monograph → Herb & supplement monograph

Ginkgo

Interacts with 1,266 drugs

Ginkgo is one of the world's most popular herbal supplements, mostly taken to support memory and circulation. The evidence for these uses is mixed and generally weak, and it is not proven to...

Read the full Ginkgo monograph → Herb & supplement monograph

Cowhage

Interacts with 193 drugs

Cowhage (Mucuna pruriens) is a tropical legume best known as a natural source of L-dopa, the compound the body turns into dopamine. It is most studied for Parkinson's disease symptoms and ma...

Read the full Cowhage monograph → Herb & supplement monograph

L-arginine

Interacts with 403 drugs

L-arginine is an amino acid that the body uses to make nitric oxide, a substance that helps blood vessels relax and widen. It is popularly used for blood pressure, erectile dysfunction, and...

Read the full L-arginine monograph → Herb & supplement monograph

Tribulus

Interacts with 259 drugs

Tribulus is a plant supplement most often marketed to boost libido, testosterone, and athletic performance, but the human evidence behind these claims is weak and inconsistent. It is general...

Read the full Tribulus monograph → Herb & supplement monograph

Muira Puama

Muira puama is a Brazilian plant traditionally used as an aphrodisiac and general tonic, often nicknamed 'potency wood.' Human research is very limited, so its benefits are not well proven,...

Read the full Muira Puama monograph → Herb & supplement monograph

Butea Superba

Interacts with 7 drugs

Butea superba is a Thai herb traditionally used to support male sexual health, but the human evidence is very limited and mostly small or low-quality. Its safety has not been well studied, s...

Read the full Butea Superba monograph → Herb & supplement monograph

Cordyceps

Interacts with 249 drugs

Cordyceps is a fungus used in traditional Chinese medicine for energy, exercise performance, and lung and immune support. Human research is limited and mostly low quality, so its benefits ar...

Read the full Cordyceps monograph → Herb & supplement monograph

Bitter Melon

Interacts with 282 drugs

Bitter melon is a tropical fruit eaten as food and used in traditional medicine, most often for blood sugar control. While some small studies hint it may modestly lower blood sugar, the evid...

Read the full Bitter Melon monograph → Herb & supplement monograph

Niacin

Interacts with 727 drugs

Niacin (vitamin B3) is an essential nutrient your body needs for energy and metabolism, and deficiency is uncommon in most developed countries. Prescription-strength niacin has been used to...

Read the full Niacin monograph → Herb & supplement monograph

Maca

Maca is a nutrient-rich Andean root often used for energy, libido, and menopause symptoms. Early studies suggest it may modestly help sexual desire and some menopause symptoms, but the evide...

Read the full Maca monograph → Herb & supplement monograph

Black Pepper

Interacts with 1,019 drugs

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

Read the full Black Pepper monograph → Herb & supplement monograph

Eurycoma Longifolia

Interacts with 248 drugs

Eurycoma longifolia (tongkat ali) is a Southeast Asian herb most popular for supporting testosterone, libido, and male fertility, with some small human studies suggesting possible benefits....

Read the full Eurycoma Longifolia monograph → Herb & supplement monograph

Boron

Boron is a trace mineral found in many plant foods and sold as a supplement, mainly promoted for bone, joint, and hormone health. The human evidence for most of these uses is limited or prel...

Read the full Boron monograph → Herb & supplement monograph

Horny Goat Weed

Interacts with 963 drugs

Horny goat weed (Epimedium) is a traditional Chinese herb most often marketed for low libido and erectile problems, but solid human evidence for these uses is lacking. While short-term use s...

Read the full Horny Goat Weed monograph →
Sources

Sources & How We Checked

Rize 2 The Occasion'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 492 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.

Yohimbe 66 references
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  2. McGuffin M, Hobbs C, Upton R, Goldberg A, eds. American Herbal Products Association's Botanical Safety Handbook. Boca Raton, FL: CRC Press, LLC 1997.
  3. Gruenwald J, Brendler T, Jaenicke C. PDR for Herbal Medicines. 1st ed. Montvale, NJ: Medical Economics Company, Inc., 1998.
  4. Brinker F. Herb Contraindications and Drug Interactions. 2nd ed. Sandy, OR: Eclectic Medical Publications, 1998.
  5. Milman N, Scheibel J, Jessen O. Lysine prophylaxis in recurrent herpes simplex labialis: a double-blind, controlled crossover study. Acta Derm Venereol 1980;60:85-7.
  6. Teloken C, Rhoden EL, Sogari P, et al. Therapeutic effects of high dose yohimbine hydrochloride on organic erectile dysfunction. J Urol 1998;159:122-4. PubMed
  7. Jacobsen FM. Fluoxetine-induced sexual dysfunction and an open trial of yohimbine. J Clin Psychiatry 1992;53:119-22.
  8. Hollander E, McCarley A. Yohimbine treatment of sexual side effects induced by serotonin reuptake blockers. J Clin Psychiatry 1992;53:207-9.
  9. Sandler B, Aronson P. Yohimbine-induced cutaneous drug eruption, progressive renal failure, and lupus-like syndrome. Urol 1993;41:343-5. PubMed
  10. Kearney T, Tu N, Haller C. Adverse drug events associated with yohimbine-containing products: a retrospective review of the California Poison Control System reported cases. Ann Pharmacother 2010;44:1022-9. PubMed
  11. VandenBrink, B. M., Foti, R. S., Rock, D. A., Wienkers, L. C., and Wahlstrom, J. L. Prediction of CYP2D6 drug interactions from in vitro data: evidence for substrate-dependent inhibition. Drug Metab Dispos. 2012;40(1):47-53. PubMed
  12. Abebe, W. An overview of herbal supplement utilization with particular emphasis on possible interactions with dental drugs and oral manifestations. J Dent.Hyg. 2003;77(1):37-46.
  13. Mustonen, P., Savola, J., and Lassila, R. Atipamezole, an imidazoline-type alpha(2)-adrenoceptor inhibitor, binds to human platelets and inhibits their adrenaline-induced aggregation more effectively than yohimbine. Thromb.Res 8-1-2000;99(3):231-237.
  14. Cameron, O. G., Zubieta, J. K., Grunhaus, L., and Minoshima, S. Effects of yohimbine on cerebral blood flow, symptoms, and physiological functions in humans. Psychosom.Med 2000;62(4):549-559. PubMed
  15. Bowes, M. P., Peters, R. H., Kernan, W. J., Jr., and Hopper, D. L. Effects of yohimbine and idazoxan on motor behaviors in male rats. Pharmacol.Biochem.Behav. 1992;41(4):707-713.
  16. Bagheri, H., Schmitt, L., Berlan, M., and Montastruc, J. L. Effect of 3 weeks treatment with yohimbine on salivary secretion in healthy volunteers and in depressed patients treated with tricyclic antidepressants. Br J Clin Pharmacol 1992;34(6):555-558. PubMed
  17. Bagheri, H., Bompart, G., Girolami, J. P., Montastruc, J. L., and Montastruc, P. Is yohimbine-induced increase in salivary secretion a kinin-dependent mechanism? Fundam.Clin Pharmacol 1992;6(1):17-20. PubMed
  18. Swann, A. C., Birnbaum, D., Jagar, A. A., Dougherty, D. M., and Moeller, F. G. Acute yohimbine increases laboratory-measured impulsivity in normal subjects. Biol.Psychiatry 5-15-2005;57(10):1209-1211. PubMed
  19. Adeniyi, A. A., Brindley, G. S., Pryor, J. P., and Ralph, D. J. Yohimbine in the treatment of orgasmic dysfunction. Asian J Androl 2007;9(3):403-407. PubMed
  20. Murburg, M. M., Villacres, E. C., Ko, G. N., and Veith, R. C. Effects of yohimbine on human sympathetic nervous system function. J Clin Endocrinol.Metab 1991;73(4):861-865. PubMed
  21. Giampreti, A., Lonati, D., Locatelli, C., Rocchi, L., and Campailla, M. T. Acute neurotoxicity after yohimbine ingestion by a body builder. Clin Toxicol.(Phila) 2009;47(8):827-829. PubMed
  22. Bloomer, R. J., Canale, R. E., Blankenship, M. M., Hammond, K. G., Fisher-Wellman, K. H., and Schilling, B. K. Effect of the dietary supplement Meltdown on catecholamine secretion, markers of lipolysis, and metabolic rate in men and women: a randomized,
  23. Myers, A. and Barrueto, F., Jr. Refractory priapism associated with ingestion of yohimbe extract. J Med Toxicol. 2009;5(4):223-225.
  24. Berlin, I., Crespo-Laumonnier, B., Cournot, A., Landault, C., Aubin, F., Legrand, J. C., and Puech, A. J. The alpha 2-adrenergic receptor antagonist yohimbine inhibits epinephrine-induced platelet aggregation in healthy subjects. Clin Pharmacol.Ther. 199
  25. Swann, A. C. Mechanisms of impulsivity in bipolar disorder and related illness. Epidemiol.Psichiatr.Soc. 2010;19(2):120-130.
  26. Shibao, C., Okamoto, L. E., Gamboa, A., Yu, C., Diedrich, A., Raj, S. R., Robertson, D., and Biaggioni, I. Comparative efficacy of yohimbine against pyridostigmine for the treatment of orthostatic hypotension in autonomic failure. Hypertension 2010;56(5) PubMed
  27. Soeter, M. and Kindt, M. Stimulation of the noradrenergic system during memory formation impairs extinction learning but not the disruption of reconsolidation. Neuropsychopharmacology 2012;37(5):1204-1215. PubMed
  28. Cimolai, N. and Cimolai, T. Yohimbine use for physical enhancement and its potential toxicity. J Diet.Suppl 2011;8(4):346-354. PubMed
  29. Bagheri, H., Berlan, M., Montastruc, J. L., and Montastruc, P. Yohimbine and lacrimal secretion. Br J Clin Pharmacol. 1990;30(1):151-152.
  30. Landis, E. and Shore, E. Yohimbine-induced bronchospasm. Chest 1989;96(6):1424. PubMed
  31. Susset, J. G., Tessier, C. D., Wincze, J., Bansal, S., Malhotra, C., and Schwacha, M. G. Effect of yohimbine hydrochloride on erectile impotence: a double-blind study. J Urol. 1989;141(6):1360-1363. PubMed
  32. Chatelut, E., Rispail, Y., Berlan, M., and Montastruc, J. L. Yohimbine increases human salivary secretion. Br.J Clin Pharmacol. 1989;28(3):366-368. PubMed
  33. Montastruc, P., Berlan, M., and Montastruc, J. L. Effects of yohimbine on submaxillary salivation in dogs. Br J Pharmacol 1989;98(1):101-104. PubMed
  34. Charney, D. S., Price, L. H., and Heninger, G. R. Desipramine-yohimbine combination treatment of refractory depression. Implications for the beta-adrenergic receptor hypothesis of antidepressant action. Arch.Gen.Psychiatry 1986;43(12):1155-1161. PubMed
  35. Braddock, L., Cowen, P. J., Elliott, J. M., Fraser, S., and Stump, K. Binding of yohimbine and imipramine to platelets in depressive illness. Psychol.Med 1986;16(4):765-773. PubMed
  36. Bolme, P., Corrodi, H., Fuxe, K., Hokfelt, T., Lidbrink, P., and Goldstein, M. Possible involvement of central adrenaline neurons in vasomotor and respiratory control. Studies with clonidine and its interactions with piperoxane and yohimbine. Eur J Pharm PubMed
  37. Charney, D. S., Heninger, G. R., and Sternberg, D. E. Assessment of alpha 2 adrenergic autoreceptor function in humans: effects of oral yohimbine. Life Sci 6-7-1982;30(23):2033-2041.
  38. Boon, N. A., Elliott, J. M., Grahame-Smith, D. G., John-Green, T., and Stump, K. A comparison of alpha 2-adrenoreceptor binding characteristics of intact human platelets identified by [3H]-yohimbine and [3H]- dihydroergocryptine. J Auton.Pharmacol 1983;3
  39. Andrejak, M., Ward, M., and Schmitt, H. Cardiovascular effects of yohimbine in anaesthetized dogs. Eur.J Pharmacol 10-28-1983;94(3-4):219-228. PubMed
  40. Brodde, O. E., Anlauf, M., Arroyo, J., Wagner, R., Weber, F., and Buck, K. D. Hypersensitivity of adrenergic receptors and blood-pressure response to oral yohimbine in orthostatic hypotension. N.Engl.J Med 4-28-1983;308(17):1033-1034. PubMed
  41. Charney, D. S., Heninger, G. R., and Redmond, D. E., Jr. Yohimbine induced anxiety and increased noradrenergic function in humans: effects of diazepam and clonidine. Life Sci. 7-4-1983;33(1):19-29. PubMed
  42. Knoll, L. D., Benson, R. C., Jr., Bilhartz, D. L., Minich, P. J., and Furlow, W. L. A randomized crossover study using yohimbine and isoxsuprine versus pentoxifylline in the management of vasculogenic impotence. J Urol. 1996;155(1):144-146. DOI
  43. Betz, J. M., White, K. D., and der Marderosian, A. H. Gas chromatographic determination of yohimbine in commercial yohimbe products. J AOAC Int 1995;78(5):1189-1194. DOI
  44. Bagheri, H., Chale, J. J., Guyen, L. N., Tran, M. A., Berlan, M., and Montastruc, J. L. Evidence for activation of both adrenergic and cholinergic nervous pathways by yohimbine, an alpha 2-adrenoceptor antagonist. Fundam.Clin Pharmacol 1995;9(3):248-254.
  45. Kennedy, S. H., Gnam, W., Ralevski, E., and Brown, G. M. Melatonin responses to clonidine and yohimbine challenges. J Psychiatry Neurosci. 1995;20(4):297-304.
  46. Musso, N. R., Vergassola, C., Pende, A., and Lotti, G. Yohimbine effects on blood pressure and plasma catecholamines in human hypertension. Am J Hypertens. 1995;8(6):565-571. PubMed
  47. Morgan, C. A., III, Southwick, S. M., Grillon, C., Davis, M., Krystal, J. H., and Charney, D. S. Yohimbine-facilitated acoustic startle reflex in humans. Psychopharmacology (Berl) 1993;110(3):342-346. PubMed
  48. Adler, L. E., Hoffer, L., Nagamoto, H. T., Waldo, M. C., Kisley, M. A., and Giffith, J. M. Yohimbine impairs P50 auditory sensory gating in normal subjects. Neuropsychopharmacology 1994;10(4):249-257. PubMed
  49. Biaggioni, I., Robertson, R. M., and Robertson, D. Manipulation of norepinephrine metabolism with yohimbine in the treatment of autonomic failure. J Clin Pharmacol. 1994;34(5):418-423. PubMed
  50. Kenney, W. L., Zappe, D. H., Tankersley, C. G., and Derr, J. A. Effect of systemic yohimbine on the control of skin blood flow during local heating and dynamic exercise. Am J Physiol 1994;266(2 Pt 2):H371-H376. PubMed
  51. Friesen, K., Palatnick, W., and Tenenbein, M. Benign course after massive ingestion of yohimbine. J Emerg.Med 1993;11(3):287-288. PubMed
  52. Bierer, L. M., Aisen, P. S., Davidson, M., Ryan, T. M., Stern, R. G., Schmeidler, J., and Davis, K. L. A pilot study of oral physostigmine plus yohimbine in patients with Alzheimer disease. Alzheimer Dis.Assoc.Disord. 1993;7(2):98-104. PubMed
  53. Mann, K., Klingler, T., Noe, S., Roschke, J., Muller, S., and Benkert, O. Effects of yohimbine on sexual experiences and nocturnal penile tumescence and rigidity in erectile dysfunction. Arch.Sex Behav. 1996;25(1):1-16. PubMed
  54. Rowland, D. L., Kallan, K., and Slob, A. K. Yohimbine, erectile capacity, and sexual response in men. Arch Sex Behav 1997;26(1):49-62.
  55. Bremner, J. D., Innis, R. B., Ng, C. K., Staib, L. H., Salomon, R. M., Bronen, R. A., Duncan, J., Southwick, S. M., Krystal, J. H., Rich, D., Zubal, G., Dey, H., Soufer, R., and Charney, D. S. Positron emission tomography measurement of cerebral metaboli
  56. Riley AJ, Goodman R, Kellett JM, and et al. Double blind trial of yohimbine hydrochloride in the treatment of erection inadequacy. Sexual Marital Ther 1989;4(1):17-26. DOI
  57. Cohen PA, Wang YH, Maller G, DeSouza R, Khan IA. Pharmaceutical quantities of yohimbine found in dietary supplements in the USA. Drug Test Anal. 2015 Sep 22. PubMed
  58. Ruck B, Shih RD, Marcus SM. Hypertensive crisis from herbal treatment of impotence. Am J Emerg Med. 1999;17:317-318. PubMed
  59. Wylie KR. Yohimbine and sinusitis. Br J Psychiatry. 1996;169(3):384-5. PubMed
  60. Le Corre P, Parmer RJ, Kailasam MT, et al. Human sympathetic activation by alpha2-adrenergic blockade with yohimbine: Bimodal, epistatic influence of cytochrome P450-mediated drug metabolism. Clin Pharmacol Ther. 2004;76(2):139-53.
  61. Mueller-Schoell A, Michelet R, Weinelt F, Kloft C, Mikus G. CYP2D6 phenotype explains reported yohimbine concentrations in four severe acute intoxications. Arch Toxicol. 2021. PubMed
  62. Bharucha AE, Skaar T, Andrews CN, et al Relationship of cytochrome P450 pharmacogenetics to the effects of yohimbine on gastrointestinal transit and catecholamines in healthy subjects. Neurogastroenterol Motil. 2008;20(8):891-9. PubMed
  63. Schmauss M, Laakmann G, Dieterle D. Effects of alpha 2-receptor blockade in addition to tricyclic antidepressants in therapy-resistant depression. J Clin Psychopharmacol. 1988;8(2):108-11.
  64. Haron MH, Dale O, Martin K, et al. Evaluation of the Herb-Drug Interaction Potential of Commonly Used Botanicals on the US Market with Regard to PXR- and AhR-Mediated Influences on CYP3A4 and CYP1A2. J Diet Suppl 2022. PubMed
  65. Hodapp B, Haggerty A, Feldman R, Timpe J. Intracranial hemorrhage after a single dose of Yohimbine in a chronic user of clonidine. Am J Emerg Med 2022;62:145. PubMed
  66. Vay M, Meyer MJ, Blank A, et al. Oral yohimbine as a new probe drug to predict CYP2D6 activity: results of a fixed-sequence phase I trial. Clin Pharmacokinet. 2020;59(7):927-939. PubMed

See these in context on the Yohimbe monograph →

Niacin 66 references
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  4. Guyton JR, Blazing MA, Hagar J, et al. Extended-release niacin vs gemfibrozil for the treatment of low levels of high-density lipoprotein cholesterol. Niaspan-Gemfibrozil Study Group. Arch Intern Med 2000;160:1177-84. PubMed
  5. Gibbons LW, Gonzalez V, Gordon N, Grundy S. The prevalence of side effects with regular and sustained-release nicotinic acid. Am J Med 1995;99:378-85. PubMed
  6. Whelan AM, Price SO, Fowler SF, Hainer BL. The effect of aspirin on niacin-induced cutaneous reactions. J Fam Pract 1992;34:165-8.
  7. Jungnickel PW, Maloley PA, Vander Tuin EL, et al. Effect of two aspirin pretreatment regimens on niacin-induced cutaneous reactions. J Gen Intern Med 1997;12:591-6. PubMed
  8. Capuzzi DM, Guyton JR, Morgan JM, et al. Efficacy and safety of an extended-release niacin (Niaspan): a long-term study. Am J Cardiol 1998;82:74-81;disc. 85U-6U. PubMed
  9. Gray DR, Morgan T, Chretien SD, Kashyap ML. Efficacy and safety of controlled-release niacin in dyslipoproteinemic veterans. Ann Intern Med 1994;121:252-8. PubMed
  10. McKenney JM, Proctor JD, Harris S, Chinchili VM. A comparison of the efficacy and toxic effects of sustained- vs immediate-release niacin in hypercholesterolemic patients. JAMA 1994;271:672-7. DOI
  11. Knopp RH, Alagona P, Davidson M, et al. Equivalent efficacy of a time-release form of niacin (Niaspan) given once-a-night versus plain niacin in the management of hyperlipidemia. Metabolism 1998;47:1097-104. PubMed
  12. Knopp RH. Clinical profiles of plain versus sustained-release niacin (Niaspan) and the physiologic rationale for nighttime dosing. Am J Cardiol 1998;82:24U-28U;discussion 39U-41U. PubMed
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Maca 1 reference
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Panax Ginseng 66 references
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Saw Palmetto 22 references
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  13. Thurian D, Montani M, Stickel F. Drug-induced, mixed-type hepatitis following ingestion of Cordyceps sinensis. Int J Clin Pharmacol Ther 2022;60(2):115-120. PubMed
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See these in context on the Cordyceps monograph →

Bitter Melon 18 references
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  2. Welihinda J, et al. Effect of Momordica charantia on the glucose tolerance in maturity onset diabetes. J Ethnopharmacol 1986;17:277-82. PubMed
  3. Srivastava Y, Venkatakrishna-Bhatt H, Verma Y, et al. Antidiabetic and adaptogenic properties of Momordica charantia extract: An experimental and clinical evaluation. Phytother Res 1993;7:285-9.
  4. Baldwa VS, Bhandari CM, Pangaria A, Goyal RK. Clinical trial in patients with diabetes mellitus of an insulin-like compound obtained from plant sources. Ups J Med Sci 1977;82:39-41. PubMed
  5. Aslam M, Stockley IH. Interaction between curry ingredient (karela) and drug (chlorpropamide). Lancet 1979:1:607. PubMed
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  7. Basch E, Gabardi S, Ulbricht C. Bitter melon (Momordica charantia): a review of efficacy and safety. Am J Health Syst Pharm 2003;60:356-9. PubMed
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  9. Rahman IU, Khan RU, Rahman KU, Bashir M. Lower hypoglycemic but higher antiatherogenic effects of bitter melon than glibenclamide in type 2 diabetic patients. Nutr J. 2015;14:13. PubMed
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  11. Konishi T, Satsu H, Hatsugai Y, et al. Inhibitory effect of a bitter melon extract on the P-glycoprotein activity in intestinal Caco-2 cells. Br J Pharmacol. 2004;143(3):379-87. PubMed
  12. Peter EL, Kasali FM, Deyno S, et al. Momordica charantia L. lowers elevated glycaemia in type 2 diabetes mellitus patients: Systematic review and meta-analysis. J Ethnopharmacol. 2019;231:311-24. doi: 10.1016/j.jep.2018.10.033. PubMed
  13. Cortez-Navarrete M, Mart&iacute;nez-Abundis E, P&eacute;rez-Rubio KG, Gonz&aacute;lez-Ortiz M, M&eacute;ndez-Del Villar M. Momordica charantia administration improves insulin secretion in type 2 diabetes mellitus. J Med Food. 2018;21(7):672-7. doi: 10.108
  14. Kim SK, Jung J, Jung JH, et al. Hypoglycemic efficacy and safety of Momordica charantia (bitter melon) in patients with type 2 diabetes mellitus. Complement Ther Med. 2020 Aug;52:102524. doi: 10.1016/j.ctim.2020.102524. PubMed
  15. Unsal O, Sütcüoglu O, Yazici O. Dangerous interaction of bitter melon (Momordica charantia) with pazopanib: a case of acute pancreatitis. J Oncol Pharm Pract 2022;28(2):486-8.
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See these in context on the Bitter Melon 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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