Interactions on record — worth a quick check against your medications. Based on 8 of 12 ingredients. Check your meds →
Dietary supplement

E1-Max Ingredients & Drug Interactions

by Bio-Gen Innovations

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

E1-Max is a dietary supplement by Bio-Gen Innovations with 12 active ingredients. Its ingredients are commonly taken for estrogen/hormone balance, acne and hormonal skin issues, prostate health support.Based on those ingredients, 1,409 medications have a known interaction with it, the most serious rated moderate. The ingredients most likely to interact are Quercetin, Piperine, Pomegranate extract. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.

HelloPharmacist Scorecard of E1-Max by Bio-Gen Innovations

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

From our pharmacy team — supplement deep dive

What’s inside

Low disclosure
Ingredient Transparency · database check
Low

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

Why this rating?
  • The label discloses an exact amount for 3 of its 12 active ingredients.
  • “XPE Blend” is a proprietary blend — the label gives one combined amount (265 mg) without saying how much of each component you get.

E1-Max contains 12 active ingredients. The primary ones include diindolylmethane (a compound from cruciferous vegetables), stinging nettle, piperine (from black pepper), pomegranate extract, white button mushroom extract, kaempferol, soy isoflavones, androst 3,5-dien-7,17-dione, luteolin, chrysin, cocoa extract, and quercetin.

These are combined in a capsule with inactive ingredients—silicon dioxide, magnesium stearate, dipotassium phosphate, titanium dioxide, and gelatin—which serve as fillers and binders.

Does it work?

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

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

Why this rating?
  • The label markets this product for: Male sexual health and performance support.
  • We looked for evidence on: Age-related testosterone deficiency, Erectile dysfunction (ED), Male infertility, Prostate health, Hormone balance.
  • The closest evidence on file: Pomegranate is rated "Insufficient Reliable Evidence To Rate" for Erectile dysfunction (ED) (Natural Medicines).
  • Also on file: Cocoa is rated "Insufficient Reliable Evidence To Rate" for Age-related testosterone deficiency.
  • Also on file: Chrysin is rated "Insufficient Reliable Evidence To Rate" for Male infertility.

The evidence for E1-Max's individual ingredients is limited. Diindolylmethane, stinging nettle, piperine, pomegranate, androst 3,5-dien-7,17-dione, luteolin, and chrysin all lack reliable evidence to rate them for their intended uses.

Cocoa extract shows possibly effective evidence for cardiovascular disease, and stinging nettle is possibly effective for diabetes. Quercetin and pomegranate have mixed or insufficient evidence for the conditions they're marketed for.

Overall, the data we hold does not establish that E1-Max works for any specific condition.

How safe is it?

Well-documented data
Safety Information · database check
Well characterized

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

Why this rating?
  • We hold adverse-effect (side-effect) data for 6 of the 8 matched ingredients.
  • Pregnancy & breastfeeding safety ratings cover 8 of 8.
  • General safety write-ups exist for 8 of 8.
  • Remember: this measures how much safety information exists. Thin data is not the same as being safe.

Diindolylmethane is generally well tolerated in short-term studies, but long-term safety isn't established; however, the safety data advises against it due to possible hormone effects. Common side effects include diarrhea, gas, headache, nausea, rash, and vomiting.

A rare serious effect (drug rash with eosinophilia and systemic symptoms, or DRESS) has been reported. Stinging nettle is generally well tolerated when used as directed, though one case of drug-induced liver injury has been reported.

Piperine, pomegranate, cocoa extract, and quercetin are generally well tolerated in typical food or supplement amounts, with most side effects being mild gastrointestinal (diarrhea, gas, nausea, constipation). Androst 3,5-dien-7,17-dione is a hormone-altering substance with little safety data; regulators warn against aromatase inhibitor supplements.

Chrysin appears generally well tolerated in short-term use, but long-term safety is not well studied.

Meds to double-check

Moderate interaction found
Known Interaction Concern · database check
Moderate identified

The most serious documented interaction for these ingredients is Moderate. Check your medications for a personalized result.

Why this rating?
  • 8 of the 8 matched ingredients can interact with medications — Quercetin, Pomegranate, Stinging Nettle, Black Pepper, Cocoa, among others.
  • The most serious interaction on file is rated Moderate.
  • Some involve high-stakes drug classes: anticoagulant / antiplatelet drugs; immunosuppressants / transplant drugs; diabetes medications; lithium.
  • For scale: 1,410 individual medications appear in the full list. A big number alone doesn't make a product dangerous — what matters is whether YOUR medication is on it, so run yours through the interaction checker on this page.

Before taking E1-Max, check your medications against these drug types, starting with the most serious: estrogens and hormone therapies (diindolylmethane, chrysin, and androst 3,5-dien-7,17-dione may interfere); warfarin or other blood thinners (stinging nettle, pomegranate, chrysin, and quercetin may reduce effectiveness or increase bleeding risk); antidiabetes drugs (stinging nettle may lower blood sugar further); ACE inhibitors, antihypertensive drugs, and beta-agonists (pomegranate and cocoa may amplify effects); lithium (stinging nettle may raise levels); and aromatase inhibitors (androst 3,5-dien-7,17-dione and chrysin may add effects). Piperine can raise blood levels of propranolol, phenytoin, theophylline, and several other drugs.

Quercetin interacts with OATP substrates and cyclosporine. If you're on any prescription, verify it with the tool below before you start.

Check your own medication Run your meds through the checker above

The bottom line

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

E1-Max combines several botanical and compound ingredients, but the evidence that any of them work for a specific condition is weak or absent. More importantly, it carries documented interactions with over 1,400 medications across multiple drug classes—from blood thinners and blood-pressure medications to diabetes drugs, antibiotics, and heart drugs.

If you take any prescription medication, use the checker on this page to verify your list before starting, and talk it over with your doctor or pharmacist.

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

Assessment coverage: 8 of 12 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated Jan 22, 2022.

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 E1-Max, straight from the product label.

Brand Bio-Gen Innovations
Net contents 90 Capsule(s)
Market status On market
Date entered into DSLD Jan 22, 2022
DSLD ID 264866
Product type Other Combinations
Supplement form Capsule
Dietary claims / uses All Other
Intended target group(s) Adult Male (18-50 Years)
From the label
Everything in this section is reproduced from the manufacturer’s own product label — it’s the label speaking, not HelloPharmacist. We show it so you can see exactly what the maker states; we don’t verify or endorse those statements.

Supplement Facts

The label details for E1-Max by Bio-Gen Innovations, 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)
Servings per container
90
IngredientAmount% DV
Diindolylmethane200 mg--
Stinging Nettle0 NP--
Piperine0 NP--
Pomegranate extract0 NP--
White Button Mushroom extract0 NP--
Kaempferol0 NP--
Soy Isoflavones0 NP--
Androst 3,5-dien-7,17-dione200 mg--
Luteolin0 NP--
Chrysin0 NP--
Cocoa Extract200 mg--
XPE Blend265 mg--
Quercetin0 NP--

Other ingredients: Silicon Dioxide, Magnesium Stearate, Dipotassium Phosphate, Titanium Dioxide, Gelatin

Tap any ingredient to jump to its full detail below.

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

Natural Male Supplement Complex

See for yourself

E1-Max by Bio-Gen Innovations label

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

What’s inside

The Ingredients in E1-Max by Bio-Gen Innovations

These are the 12 active ingredients this product is made of. Select any to open its full monograph.

Serving size1 Capsule(s) Dosage formCapsule Servings per container90 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.

Diindolylmethane

Interacts with
269 drugs
200 mg per serving

Diindolylmethane (DIM) is a compound made when your body digests cruciferous vegetables, and it is sold as a supplement mainly for hormone balance and...

Diindolylmethane monograph & interactions

Androst 3,5-dien-7,17-dione

Interacts with
4 drugs
200 mg per serving

Arimistane (sometimes sold as Estrovade) is a synthetic aromatase inhibitor marketed as a dietary supplement to lower estrogen and raise testosterone,...

Androst 3,5-dien-7,17-dione monograph & interactions

Cocoa Extract

Interacts with
661 drugs
200 mg per serving Form: Epicatechin

Cocoa is rich in plant compounds called flavanols that may modestly support blood vessel function and blood pressure, but most chocolate products are...

Cocoa Extract monograph & interactions

XPE Blend

265 mg per serving

Other (inactive) ingredients: Silicon Dioxide, Magnesium Stearate, Dipotassium Phosphate, Titanium Dioxide, Gelatin. These complete the product’s ingredient list but are not active constituents.

Interaction report

E1-Max by Bio-Gen Innovations Drug Interactions

Want to check YOUR meds against E1-Max?

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
1,409Drugs
1,352 Moderate 57 Minor

Ingredients driving the most interactions

Quercetin 1,169
Piperine 1,019
Chrysin 358

Each ingredient & the kinds of drugs it affects

For each ingredient in E1-Max 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.

Quercetin21 drug types · 1,169 drugs

Antidiabetes Drugs

Theoretically, concomitant use of quercetin and antidiabetes drugs might increase the risk of hypoglycemia.

Clinical research suggests that a combination of quercetin, myricetin, and chlorogenic acid reduce levels of fasting glucose in patients with type 2 diabetes, including those already taking antidiabetes agents. The effect of quercetin alone is unknown.

Likelihood Possible Evidence B
Antihypertensive Drugs

Theoretically, taking quercetin with antihypertensive drugs might increase the risk of hypotension.

Quercetin can modestly decrease blood pressure in people with mild hypertension. Theoretically, it might have additive blood pressure lowering effects when used with antihypertensive drugs.

Likelihood Possible Evidence B
Cyclosporine (Neoral, Sandimmune)

Theoretically, concomitant use might increase the levels and adverse effects of cyclosporine.

A small study in healthy volunteers shows that pretreatment with quercetin increases plasma levels and prolongs the half-life of a single dose of cyclosporine, possibly due to inhibition of p-glycoprotein or cytochrome P450 3A4 (CYP3A4), which metabolizes cyclosporin.

Likelihood Possible Evidence B
Cytochrome P450 2C8 (Cyp2C8) Substrates

Theoretically, concomitant use might increase the levels and adverse effects of CYP2C8 substrates.

In vitro research shows that quercetin inhibits CYP2C8. Inhibition of paclitaxel (Taxol) metabolism via CYP2C8 has been reported in vitro. However, a small study in humans found no effect of quercetin on rosiglitazone (Avandia), which is also a CYP2C8 substrate.

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

Theoretically, concomitant use might increase the levels and adverse effects of CYP2C9 substrates.

A small clinical study in healthy volunteers shows that taking quercetin 500 mg twice daily for 10 days prior to taking diclofenac, a CYP2C9 substrate, increases diclofenac plasma levels by 75% and prolongs the half-life by 32.5%. Animal research also shows that pretreatment with quercetin increases plasma levels and prolongs the half-life of losartan (Cozaar), a substrate of CYP2C9. Furthermore, laboratory research shows that quercetin inhibits CYP2C9.

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

Theoretically, concomitant use might increase the levels and adverse effects of CYP2D6 substrates.

In vitro research show that quercetin inhibits CYP2D6. This effect has not been reported in humans.

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

Theoretically, concomitant use might alter the effects and adverse effects of CYP3A4 substrates.
A small clinical study in healthy volunteers shows that pretreatment with quercetin increases plasma levels and prolongs the half-life of a single dose of cyclosporine (Neoral, Sandimmune), a substrate of CYP3A4. Animal research also shows that pretreatment with quercetin increases plasma levels and prolongs the half-life of losartan (Cozaar) and quetiapine (Seroquel), substrates of CYP3A4. Other laboratory research also shows that quercetin inhibits CYP3A4. However, one clinical study shows that quercetin can increase the metabolism of midazolam, a substrate of CYP3A4, and decrease serum concentrations of midazolam by about 24% in some healthy individuals, suggesting possible induction of CYP3A4.

Likelihood Possible Evidence D
Diclofenac (Voltaren, Others)

Theoretically, concomitant use might increase the levels and adverse effects of diclofenac.

A small clinical study in healthy volunteers shows that taking quercetin 500 mg twice daily for 10 days prior to taking diclofenac increases diclofenac plasma levels by 75% and prolongs the half-life by 32.5%. This is thought to be due to inhibition of CYP2C9 by quercetin.

Likelihood Probable Evidence B
Losartan (Cozaar)

Theoretically, concomitant use might increase the effects and adverse effects of losartan and decrease the effects of its active metabolite.

Animal research shows that pretreatment with quercetin increases plasma levels and prolongs the half-life of losartan (Cozaar) while decreasing plasma levels of losartan's active metabolite. This metabolite, which is around 10-fold more potent than losartan, is the result of cytochrome P450 (CYP) 2C9- and CYP3A4-mediated transformation of losartan. Additionally, in vitro research shows that quercetin may inhibit P-glycoprotein-mediated efflux of losartan from the intestines, resulting in increased absorption of losartan. These results suggest that concomitant use of quercetin and losartan might increase systemic exposure to losartan while also decreasing plasma concentrations of losartan's active and more potent metabolite.

Likelihood Possible Evidence D
Midazolam (Versed)

Theoretically, concomitant use might decrease the levels and effects of midazolam.

A small clinical study in healthy volunteers shows that quercetin can increase the metabolism of midazolam, with a decrease in AUC of about 24%.

Likelihood Possible Evidence B
Mitoxantrone

Theoretically, quercetin might increase the effects and adverse effects of mitoxantrone.
In vitro research shows that quercetin increases the intracellular accumulation and cytotoxicity of mitoxantrone, possibly through inhibition of breast cancer resistance protein (BCRP), of which mitoxantrone is a substrate. So far, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Organic Anion Transporter 1 (Oat1) Substrates

Theoretically, concomitant use might increase the effects and adverse effects of OAT1 substrates.

In vitro research shows that quercetin is a strong non-competitive inhibitor of OAT1, with half-maximal inhibitory concentration (IC50) values less than 10 mcM. So far, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Organic Anion Transporter 3 (Oat3) Substrates

Theoretically, concomitant use might increase the effects and adverse effects of OAT3 substrates.

In vitro research shows that quercetin is a strong non-competitive inhibitor of OAT3, with half-maximal inhibitory concentration (IC50) values as low as 0.75 mcM. So far, this interaction has not been reported in humans.

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

Theoretically, concomitant use might increase the effects and adverse effects of OATP substrates.

In vitro evidence shows that quercetin can inhibit organic anion-transporting peptide (OATP) 1B1-mediated uptake of estrone-3-sulfate and pravastatin. Furthermore, clinical research in healthy males shows that intake of quercetin along with pravastatin increases the AUC of pravastatin by 24%, prolongs its half-life by 14%, and decreases its apparent clearance by 18%, suggesting that quercetin modestly inhibits the uptake of pravastatin in hepatic cells.

Likelihood Possible Evidence B
P-Glycoprotein Substrates

Theoretically, concomitant use might alter the effects and adverse effects of P-glycoprotein substrates.

There is preliminary evidence that quercetin inhibits the gastrointestinal P-glycoprotein efflux pump, which might increase the bioavailability and serum levels of drugs transported by the pump. A small study in healthy volunteers reported that pretreatment with quercetin increased bioavailability and plasma levels after a single dose of cyclosporine (Neoral, Sandimmune). Also, two small studies have shown that quercetin might decrease the absorption of talinolol, a substrate transported by the gastrointestinal P-glycoprotein efflux pump. However, in another small study, several days of quercetin treatment did not significantly affect the pharmacokinetics of saquinavir (Invirase). The reason for these discrepancies is not entirely clear. Until more is known, use quercetin cautiously in combination with P-glycoprotein substrates.

Likelihood Possible Evidence B
Pravastatin (Pravachol)

Theoretically, concomitant use might increase the effects and adverse effects of pravastatin.
In vitro evidence shows that quercetin can inhibit OATP 1B1-mediated uptake of pravastatin. Also, preliminary clinical research in healthy males shows that intake of quercetin along with pravastatin increases the maximum concentration of pravastatin by 24%, prolongs its half-life by 14%, and decreases its apparent clearance by 18%, suggesting that quercetin modestly inhibits the uptake of pravastatin in hepatic cells.

Likelihood Possible Evidence B
Prazosin (Minipress)

Theoretically, quercetin might increase the effects and adverse effects of prazosin.
In vitro research shows that quercetin inhibits the transcellular efflux of prazosin, possibly through inhibition of breast cancer resistance protein (BCRP), of which prazosin is a substrate. BCRP is an ATP-binding cassette efflux transporter in the intestines, kidneys, and liver. So far, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Quetiapine (Seroquel)

Theoretically, concomitant use might increase the effects and adverse effects of quetiapine.
Animal research shows that pretreatment with quercetin can increase plasma levels of quetiapine and prolong its clearance, possibly due to inhibition of cytochrome P450 3A4 (CYP3A4) by quercetin. Additionally, the brain-to-plasma ratio of quetiapine concentrations increased, possibly due to inhibition of P-glycoprotein at the blood-brain barrier. This interaction has not been reported in humans.

Likelihood Possible Evidence D
Quinolone Antibiotics

Theoretically, concomitant use might inhibit the effects of quinolone antibiotics.
In vitro, quercetin binds to the DNA gyrase site on bacteria, which may interfere with the activity of quinolone antibiotics.

Likelihood Possible Evidence B
Sulfasalazine (Azulfidine)

Theoretically, quercetin might increase the effects and adverse effects of sulfasalazine.
Animal research shows that quercetin increases the maximum serum concentration (Cmax) and area under the curve (AUC) of sulfasalazine, possibly through inhibition of breast cancer resistance protein (BCRP), of which sulfasalazine is a substrate. So far, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Theoretically, quercetin may increase the risk of bleeding if used with warfarin.
Animal and in vitro studies show that quercetin might increase serum levels of warfarin. Quercetin and warfarin have the same human serum albumin (HSA) binding site, and in vitro research shows that quercetin has stronger affinity for the HSA binding site and can theoretically displace warfarin, causing higher serum levels of warfarin. Animal research shows that taking quercetin for 2 weeks before initiating warfarin increases the maximum serum level of warfarin by 30%, the half-life by 10%, and the overall exposure by 63% when compared with control. Concomitant administration of quercetin and warfarin, without quercetin pre-treatment, also increased these measures, but to a lesser degree. Researchers theorize that inhibition of CYP3A4 by quercetin may explain these effects. So far, this interaction has not been reported in humans.

Likelihood Possible Evidence D

Piperine17 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

Pomegranate extract9 drug types · 922 drugs

Ace Inhibitors (Aceis)

Theoretically, taking pomegranate with ACEIs might increase the risk of adverse effects.
Pomegranate juice is thought to have ACE inhibitor-like effects.

Likelihood Possible Evidence B
Antihypertensive Drugs

Theoretically, taking pomegranate with antihypertensive drugs might increase the risk of hypotension.
Consuming pomegranate juice can modestly lower blood pressure.

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

Theoretically, pomegranate might increase levels of drugs metabolized by CYP2D6.
In vitro, pomegranate juice inhibits CYP2D6. However, the clinical significance of this potential interaction in humans is not known.

Likelihood Possible Evidence D
Rosuvastatin (Crestor)

Theoretically, taking pomegranate with rosuvastatin might increase the risk of adverse effects.
In one case, a patient taking rosuvastatin 5 mg every other day in combination with ezetimibe 10 mg daily developed rhabdomyolysis after drinking pomegranate juice 200 mL twice weekly for 3 weeks. This patient had a history of elevated creatine kinase levels while not receiving any statin treatment. This suggests a possible underlying myopathy and predisposition to rhabdomyolysis.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Theoretically, pomegranate might increase warfarin levels and increase the risk of bleeding. Also, discontinuing regular consumption of pomegranate juice might decrease warfarin levels.
In one case report, a patient had a stable, therapeutic bleeding time, as measured by international normalized ratio (INR), while taking warfarin in combination with pomegranate juice 2-3 times per week. The patient became subtherapeutic within about 10 days after discontinuing pomegranate juice, which required a warfarin dose increase. In another case report, a patient with a stable INR for over one year presented with an INR of 14. The patient noted no changes to medications or diet but did report consuming around 3 liters of pomegranate juice over the previous week. The patient's INR stabilized upon moderation of pomegranate juice consumption. The mechanism of this potential interaction is unclear.

Likelihood Possible Evidence D
Carbamazepine (Tegretol)

Theoretically, taking pomegranate with carbamazepine might increase the risk of adverse effects, although research suggests this interaction is unlikely to be clinically significant.
Animal research shows that pomegranate juice may inhibit cytochrome P450 3A4 (CYP3A4) metabolism of carbamazepine and increase levels of carbamazepine by 1.5 times without prolonging the elimination half-life. This suggests that pomegranate juice inhibits intestinal CYP3A4, but might not inhibit hepatic CYP3A4. However, some human research suggests that pomegranate does not significantly inhibit CYP3A4 drug metabolism in humans.

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

Theoretically, pomegranate might increase levels of drugs metabolized by CYP2C9.
Some animal and in vitro research shows that pomegranate juice inhibits intestinal, but not hepatic, CYP2C9 isoenzyme activity. However, clinical research shows that neither pomegranate juice nor pomegranate extract have a significant effect on CYP2C9 activity in humans.

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

Theoretically, pomegranate might increase levels of drugs metabolized by CYP3A4, but most research suggests this interaction is unlikely to be clinically significant.
Pomegranate contains several polyphenols that have individually been shown to inhibit CYP3A4. However, there is contradictory evidence about the effect of whole pomegranate juice on CYP3A4 activity. In vitro, pomegranate juice significantly inhibits the CYP3A4 enzyme, with comparable inhibition to grapefruit juice. In an animal model, pomegranate juice inhibits CYP3A4 metabolism of carbamazepine and increases levels of carbamazepine by 1.5 times; however, in human volunteers, drinking a single glass of pomegranate juice 240 mL or taking 200 mL daily for 2 weeks does not significantly affect levels of the CYP3A4 substrate midazolam after oral or intravenous administration. Another study in healthy volunteers shows that consuming pomegranate juice 300 mL three times daily for three days also does not significantly affect levels of simvastatin, a CYP3A4 substrate This suggests that pomegranate is unlikely to significantly affect levels of CYP3A4 substrates in humans.

Likelihood Unlikely Evidence B
Tolbutamide (Orinase)

Theoretically, pomegranate might increase levels of tolbutamide, although research suggests this interaction is unlikely to be clinically significant.
Animal research shows that pomegranate juice inhibits the cytochrome P450 2C9 (CYP2C9) metabolism of tolbutamide. Pomegranate juice increased tolbutamide levels by 1.2 times without prolonging the elimination half-life. This suggests that pomegranate juice inhibits intestinal CYP2C9, but might not inhibit hepatic CYP2C9. Despite this evidence, clinical research shows that neither pomegranate juice nor pomegranate extract have a significant effect on CYP2C9 activity in humans. This interaction does not appear to be clinically significant in humans.

Likelihood Unlikely Evidence D

Cocoa Extract37 drug types · 661 drugs

Ace Inhibitors (Aceis)

Theoretically, taking cocoa with ACEIs might increase the risk of adverse effects.
Human research shows that dark chocolate can inhibit ACE. Additionally, prolonged angioedema in an elderly patient on an ACE inhibitor was precipitated with intake of diabetic chocolate.

Likelihood Possible Evidence D
Adenosine (Adenocard)

Theoretically, cocoa might decrease the vasodilatory effects of adenosine and interfere with its use prior to stress testing.
Cocoa contains caffeine. Caffeine is a competitive inhibitor of adenosine at the cellular level. However, caffeine does not seem to affect supplemental adenosine because high interstitial levels of adenosine overcome the antagonistic effects of caffeine. It is recommended that methylxanthines and methylxanthine-containing products be stopped 24 hours prior to pharmacological stress tests. However, methylxanthines appear more likely to interfere with dipyridamole than adenosine-induced stress testing.

Likelihood Possible Evidence B
Alcohol (Ethanol)

Theoretically, concomitant use might increase levels and adverse effects of caffeine.
Cocoa contains caffeine. Alcohol reduces caffeine metabolism. Concomitant use of alcohol can increase caffeine serum concentrations and the risk of caffeine adverse effects.

Likelihood Probable Evidence D
Anticoagulant/Antiplatelet Drugs

Theoretically, cocoa may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
Clinical research shows that intake of cocoa can inhibit platelet adhesion, aggregation, and activity and increase aspirin-induced bleeding time. For patients on dual antiplatelet therapy, cocoa may enhance the inhibitory effect of clopidogrel, but not aspirin, on platelet aggregation.

Likelihood Possible Evidence D
Antihypertensive Drugs

Theoretically, taking cocoa with antihypertensive drugs might increase the risk of hypotension.
Clinical research shows that cocoa can modestly decrease blood pressure in hypertensive and normotensive patients.

Likelihood Possible Evidence D
Beta-Adrenergic Agonists

Theoretically, large amounts of cocoa might increase the cardiac inotropic effects of beta-agonists.
Cocoa contains caffeine. Theoretically, large amounts of caffeine might increase cardiac inotropic effects of beta-agonists. A case of atrial fibrillation associated with consumption of large quantities of chocolate in a patient with chronic albuterol inhalation abuse has also been reported.

Likelihood Probable Evidence D
Cytochrome P450 1A2 (Cyp1A2) Inhibitors

Theoretically, concomitant use might increase the levels and adverse effects of caffeine.
Cocoa contains caffeine. Caffeine is metabolized by cytochrome P450 1A2 (CYP1A2),. Theoretically, drugs that inhibit CYP1A2 may decrease the clearance rate of caffeine from cocoa and increase caffeine levels.

Likelihood Possible Evidence D
Dipyridamole (Persantine)

Theoretically, cocoa might decrease the vasodilatory effects of dipyridamole and interfere with its use prior to stress testing.
Cocoa contains caffeine. Caffeine may inhibit dipyridamole-induced vasodilation. It is recommended that methylxanthines and methylxanthine-containing products be stopped 24 hours prior to pharmacological stress tests. Methylxanthines appear more likely to interfere with dipyridamole than adenosine-induced stress testing.

Likelihood Probable Evidence B
Disulfiram (Antabuse)

Theoretically, disulfiram might increase the risk of adverse effects from caffeine.
Cocoa contains caffeine. In human research, disulfiram decreases the rate of caffeine clearance.

Likelihood Probable Evidence B
Diuretic Drugs

Theoretically, using cocoa with diuretic drugs might increase the risk of hypokalemia.
Cocoa contains caffeine. In excessive amounts, caffeine can reduce potassium levels due to stimulation of the sodium-potassium pump. Diuretics can also cause lower potassium levels.

Likelihood Possible Evidence D
Ephedrine

Theoretically, concomitant use might increase the risk for stimulant adverse effects.
Cocoa contains caffeine. There is evidence that using ephedrine with caffeine might increase the risk of serious life-threatening or debilitating adverse effects such as hypertension, myocardial infarction, stroke, seizures, and death.

Likelihood Possible Evidence D
Estrogens

Theoretically, estrogens might increase the levels and adverse effects of caffeine.
Cocoa contains caffeine. Estrogen inhibits caffeine metabolism.

Likelihood Probable Evidence B
Flutamide (Eulexin)

Theoretically, cocoa might increase the levels and adverse effects of flutamide.
Cocoa contains caffeine. In vitro evidence suggests that caffeine can inhibit the metabolism of flutamide.

Likelihood Possible Evidence D
Fluvoxamine (Luvox)

Theoretically, fluvoxamine might increase the levels and adverse effects of caffeine.
Cocoa contains caffeine. Fluvoxamine reduces caffeine metabolism.

Likelihood Probable Evidence D
Lithium

Theoretically, abrupt cocoa withdrawal might increase the levels and adverse effects of lithium.
Cocoa contains caffeine. There are two case reports of lithium tremor that worsened upon abrupt coffee withdrawal.

Likelihood Possible Evidence D
Monoamine Oxidase Inhibitors (Maois)

Theoretically, concomitant use might increase the risk of a hypertensive crisis.
Cocoa contains caffeine. Large amounts of caffeine with MAOIs might precipitate a hypertensive crisis.

Likelihood Possible Evidence D
Nicotine

Theoretically, concomitant use might increase the risk of hypertension.
Cocoa contains caffeine. Concomitant use of caffeine and nicotine has been shown to have additive cardiovascular effects, including increased heart rate and blood pressure. Blood pressure was increased by 10.8/12.4 mmHg when the agents were used concomitantly.

Likelihood Probable Evidence B
Pentobarbital (Nembutal)

Theoretically, cocoa might decrease the effects of pentobarbital.
Cocoa contains caffeine. Caffeine might negate the hypnotic effects of pentobarbital.

Likelihood Possible Evidence B
Phenobarbital (Luminal)

Theoretically, cocoa might reduce the effects of phenobarbital and increase the risk for convulsions.
Cocoa contains caffeine. Animal research suggests that caffeine can decrease the anticonvulsant activity of phenobarbital. The exact mechanism of this interaction is unclear.

Likelihood Possible Evidence D
Phenylpropanolamine

Theoretically, phenylpropanolamine might increase the risk of hypertension, as well as the levels and adverse effects of caffeine.
Cocoa contains caffeine. Concomitant use of phenylpropanolamine and caffeine might cause an additive increase in blood pressure. Phenylpropanolamine also seems to increase caffeine serum levels.

Likelihood Probable Evidence B
Phenytoin (Dilantin)

Theoretically, cocoa might reduce the effects of phenytoin and increase the risk for convulsions.
Cocoa contains caffeine. Animal research suggests that caffeine can decrease the anticonvulsant activity of phenytoin. The effect does not seem to be related to the seizure threshold-lowering effects of caffeine. However, the exact mechanism of this interaction is unclear.

Likelihood Possible Evidence D
Quinolone Antibiotics

Theoretically, quinolone antibiotics might increase the levels and adverse effects of caffeine.
Cocoa contains caffeine. Quinolones (also referred to as fluoroquinolones) decrease caffeine clearance.

Likelihood Probable Evidence B
Riluzole (Rilutek)

Theoretically, concomitant use might increase the levels and adverse effects of both caffeine and riluzole.
Cocoa contains caffeine. Caffeine and riluzole are both metabolized by cytochrome P450 1A2, and concomitant use might reduce metabolism of one or both agents.

Likelihood Possible Evidence D
Stimulant Drugs

Theoretically, concomitant use might increase stimulant adverse effects.
Cocoa contains caffeine. Concomitant use might increase the risk of stimulant adverse effects.

Likelihood Probable Evidence C
Theophylline

Theoretically, cocoa might increase the levels and adverse effects of theophylline.
Cocoa contains caffeine. Large amounts of caffeine might inhibit theophylline metabolism. Caffeine decreases theophylline clearance 23% to 29%.

Likelihood Probable Evidence B

Chrysin9 drug types · 358 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, chrysin might increase the risk of bleeding when taken with anticoagulant or antiplatelet drugs.
In vitro evidence suggests that chrysin might inhibit platelet aggregation.

Likelihood Possible Evidence D
Aromatase Inhibitors

Theoretically, chrysin might increase the effects and adverse effects of aromatase inhibitors.
In vitro research suggests that chrysin might decrease estrogen synthesis by acting as an aromatase (estrogen synthetase) inhibitor..

Likelihood Possible Evidence D
Contraceptive Drugs

Theoretically, chrysin might reduce the efficacy of estrogen-containing contraceptive drugs.
In vitro research suggests that chrysin might have antiestrogenic activity.

Likelihood Possible Evidence D
Diclofenac (Voltaren, Others)

Theoretically, chrysin might increase the effects and adverse effects of diclofenac.
In vitro research suggests that chrysin and its sulfate conjugate inhibit diclofenac metabolism. It is speculated that chrysin and its sulfate conjugate reduce the metabolism of diclofenac by inhibiting cytochrome P450 2C9. This effect has not been reported in humans.

Likelihood Possible Evidence D
Estrogens

Theoretically, chrysin might decrease the effects of estrogen therapy.
In vitro research suggests that chrysin might have antiestrogenic activity.

Likelihood Possible Evidence D
Mephenytoin (Mesantoin)

Theoretically, chrysin might increase the effects and adverse effects of mephenytoin.
In vitro research suggests that chrysin and its sulfate and glucuronide conjugates inhibit S-mephenytoin metabolism. It is speculated that chrysin and its conjugates reduce the metabolism of S-mephenytoin by inhibiting cytochrome P450 2C19. This effect has not been reported in humans.

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

Theoretically, chrysin might increase levels of drugs metabolized by CYP1A2.
In vitro research suggests that chrysin inhibits CYP1A2 isozymes. However, chrysin does not appear to inhibit CYP1A2-dependent caffeine metabolism in animals. Due to chrysin's low bioavailability and rapid metabolism to glucuronide and sulfate conjugates, this interaction is unlikely.

Likelihood Unlikely Evidence D
Glucuronidated Drugs

Theoretically, chrysin might increase the clearance of drugs that are UGT1A1 substrates, thereby reducing their effectiveness.
In vitro research suggests that chrysin might induce UDP-glucuronosyltransferase 1A1 (UGT1A1).

Likelihood Unlikely Evidence D
Testosterone

Theoretically, chrysin might increase the effects and adverse effects of testosterone.
In vitro research suggests that chrysin and its sulfate conjugate inhibit testosterone metabolism. It is speculated that chrysin and its sulfate conjugate reduce the metabolism of testosterone by inhibiting cytochrome P450 3A4. This effect has not been reported in humans.

Likelihood Possible Evidence D

Diindolylmethane3 drug types · 269 drugs

Diuretic Drugs

Theoretically, diindolylmethane might increase the risk of hyponatremia if used with sodium-depleting diuretics.
Large doses of diindolylmethane (600 mg daily) have been associated with two cases of asymptomatic hyponatremia in clinical research.

Likelihood Possible Evidence B
Estrogens

Theoretically, diindolylmethane might increase or decrease the effects of estrogens.
Diindolylmethane might have mild estrogenic or antiestrogenic effects. Theoretically, large amounts of diindolylmethane might interfere with hormone replacement therapy.

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

Theoretically, diindolylmethane might lower serum levels of CYP1A2 substrates.
In vitro evidence suggests that diindolylmethane can induce CYP1A2. Theoretically, it might increase metabolism of CYP1A2 substrates and lower serum concentrations. This interaction has not been reported in humans.

Likelihood Unlikely Evidence D

Stinging Nettle4 drug types · 164 drugs

Antidiabetes Drugs

Theoretically, stinging nettle might have additive effects with antidiabetes drugs.
Clinical research shows that stinging nettle might decrease blood glucose levels in patients with diabetes.

Likelihood Possible Evidence B
Diuretic Drugs

Theoretically, combining stinging nettle with diuretic drugs may have additive effects.
Animal research suggests that the above ground parts and roots of stinging nettle may have a diuretic effect.

Likelihood Possible Evidence D
Lithium

Theoretically, stinging nettle might reduce excretion and increase levels of lithium.
Animal research suggests that stinging nettle has diuretic and natriuretic properties, which could alter the excretion of lithium. The dose of lithium might need to be decreased.

Likelihood Possible Evidence D
Warfarin (Coumadin)

There is some concern that stinging nettle might decrease the effects of anticoagulant drugs such as warfarin.
Stinging nettle contains a significant amount of vitamin K. When taken in large quantities, this might interfere with the activity of warfarin.

Likelihood Possible Evidence D

Androst 3,5-dien-7,17-dione1 drug type · 4 drugs

Aromatase Inhibitors

It is believed that Arimistane inhibits the aromatase enzyme, which may interact with other aromatase inhibitors. This interaction could potentially increase the risk of side effects associated with low estrogen levels or from additive side effects, such as an increased risk of liver toxicity. It is recommended to consult with a healthcare provider before combining Arimistane with other aromatase inhibitors to assess the potential risks and benefits.

Likelihood Probable Evidence C
The maker

Brand information

Manufacturer and brand details for E1-Max, from the product label.

Bio-Gen Innovations

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Name
Bio-Gen Innovations
Pharmacist Counseling Corner

E1-Max by Bio-Gen Innovations: Common Questions

Does E1-Max by Bio-Gen Innovations interact with any medications?
Yes. Based on its ingredients, E1-Max has a known interaction with 1,409 medications. Use the checker to see how it interacts with a specific drug.
How can one product interact with so many drugs?
E1-Max contains 12 active ingredients, and an interaction can come from any of them. We check every ingredient, combine the results into one list per medication, and show which ingredient and mechanism is responsible.
Where does this information come from?
The product label data comes from the NIH Dietary Supplement Label Database (DSLD); the interaction data is built on the Natural Medicines database and reviewed by HelloPharmacist pharmacists.
Is E1-Max safe during pregnancy?
Not for all of it. Diindolylmethane is rated likely safe, and piperine and pomegranate are possibly safe, but stinging nettle is rated likely unsafe during pregnancy. Androst 3,5-dien-7,17-dione is possibly unsafe because lowering estrogen in pregnancy could be harmful. The safety data for several other ingredients (kaempferol, soy isoflavones, luteolin, chrysin, cocoa extract, quercetin) is either absent or incomplete. This product is not recommended in pregnancy; talk to your doctor before using it.
Can I take this while breastfeeding?
We don't have enough safety data to recommend it. Stinging nettle and androst 3,5-dien-7,17-dione should be avoided while breastfeeding. Diindolylmethane, piperine, pomegranate, and cocoa extract may be okay, but safety information for the others is not on file. Since this is a multi-ingredient product and some components carry real concerns, talk with your doctor or pharmacist before nursing.
What are the most common side effects?
Gastrointestinal effects dominate: diarrhea, gas, nausea, constipation, and bloating appear across several ingredients. Headache, rash, and vomiting have been reported with diindolylmethane. Cocoa extract's caffeine can cause headache, nausea, and gastrointestinal upset. Most of these are mild, but if they persist or worsen, stop and check with your pharmacist.
Does E1-Max actually work for anything?
The evidence is weak. Cocoa extract is possibly effective for cardiovascular disease, and stinging nettle is possibly effective for diabetes. The other ingredients lack reliable evidence to rate them. We can't tell you this product will work for any specific health goal based on the data we hold.
Which ingredients can I not find interaction data for?
We could not check white button mushroom extract, kaempferol, soy isoflavones, or luteolin for drug interactions. If you're concerned about those ingredients specifically, ask your pharmacist or doctor whether they might affect your medications.
Why does E1-Max interact with so many drugs?
Because it contains 12 active ingredients, each of which can affect how your body absorbs, metabolizes, or eliminates medications. Piperine slows how your liver breaks down many drugs, raising their blood levels. Quercetin, pomegranate, and chrysin inhibit similar enzyme pathways. Diindolylmethane can speed up liver metabolism and lower levels of some drugs. Stinging nettle acts as a diuretic and contains vitamin K. Even one ingredient can affect dozens of medications; together, they span over 1,400. That's why checking your own prescriptions is essential.

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

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

E1-Max label
Go deeper

The Full Monographs Behind E1-Max’s Ingredients

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

Herb & supplement monograph

Diindolylmethane

Interacts with 269 drugs

Diindolylmethane (DIM) is a compound made when your body digests cruciferous vegetables, and it is sold as a supplement mainly for hormone balance and cancer prevention. Although early lab s...

Read the full Diindolylmethane monograph →
Herb & supplement monograph

Arimistane

Interacts with 4 drugs

Arimistane (sometimes sold as Estrovade) is a synthetic aromatase inhibitor marketed as a dietary supplement to lower estrogen and raise testosterone, often during or after steroid or prohor...

Read the full Arimistane monograph →
Herb & supplement monograph

Cocoa

Interacts with 661 drugs

Cocoa is rich in plant compounds called flavanols that may modestly support blood vessel function and blood pressure, but most chocolate products are high in sugar, fat, and calories, which...

Read the full Cocoa monograph →
Herb & supplement monograph

Stinging Nettle

Interacts with 164 drugs

Stinging nettle is a common plant used as food and in traditional medicine, most often for prostate symptoms, allergies, and joint pain. The evidence is mixed and mostly preliminary, so it i...

Read the full Stinging Nettle 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

Pomegranate

Interacts with 922 drugs

Pomegranate is a nutrient-rich fruit that is high in antioxidants and is widely enjoyed as food and juice. Early research suggests it may support heart health and blood pressure, but the evi...

Read the full Pomegranate monograph →
Herb & supplement monograph

Chrysin

Interacts with 358 drugs

Chrysin is a plant flavonoid sold mainly as a bodybuilding supplement claimed to raise testosterone or block estrogen, but human studies have not shown these benefits, largely because the bo...

Read the full Chrysin monograph →
Herb & supplement monograph

Quercetin

Interacts with 1,169 drugs

Quercetin is a plant flavonoid with antioxidant and anti-inflammatory properties found in many common foods and sold as a supplement. While early research is interesting for allergies, blood...

Read the full Quercetin monograph →
Sources

Sources & How We Checked

E1-Max'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 262 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.

Diindolylmethane 14 references
  1. Natl Inst Health, Natl Inst Environmental Health Sci. Indole-3-carbinol. Available at: http://ntp-server.niehs.nih.gov.
  2. Balk JL. Indole-3-carbinol for cancer prevention. Altern Med Alert 2000; 3:105-7.
  3. Riby JE, Chang GHF, Firestone GL, Bjeldanes LF. Ligand-independent activation of estrogen receptor function by 3,3'-diindolylmethane in human breast cancer cells. Biochem Pharmacol 2000;60:167-77. PubMed
  4. Lake BG, Tredger JM, Renwick AB, et al. 3'3-diindolylmethane induces CYP1A2 in cultured precision-cut human liver slices. Xenobiotica 1998;28:803-11. PubMed
  5. Dalessandri, K. M., Firestone, G. L., Fitch, M. D., Bradlow, H. L., and Bjeldanes, L. F. Pilot study: effect of 3,3'-diindolylmethane supplements on urinary hormone metabolites in postmenopausal women with a history of early-stage breast cancer. Nutr Canc PubMed
  6. Reed, G. A., Arneson, D. W., Putnam, W. C., Smith, H. J., Gray, J. C., Sullivan, D. K., Mayo, M. S., Crowell, J. A., and Hurwitz, A. Single-dose and multiple-dose administration of indole-3-carbinol to women: pharmacokinetics based on 3,3'-diindolylmetha
  7. Reed, G. A., Sunega, J. M., Sullivan, D. K., Gray, J. C., Mayo, M. S., Crowell, J. A., and Hurwitz, A. Single-dose pharmacokinetics and tolerability of absorption-enhanced 3,3'-diindolylmethane in healthy subjects. Cancer Epidemiol.Biomarkers Prev. 2008; PubMed
  8. Del Priore G., Gudipudi, D. K., Montemarano, N., Restivo, A. M., Malanowska-Stega, J., and Arslan, A. A. Oral diindolylmethane (DIM): pilot evaluation of a nonsurgical treatment for cervical dysplasia. Gynecol.Oncol. 2010;116(3):464-467. PubMed
  9. Heath, E. I., Heilbrun, L. K., Li, J., Vaishampayan, U., Harper, F., Pemberton, P., and Sarkar, F. H. A phase I dose-escalation study of oral BR-DIM (BioResponse 3,3'- Diindolylmethane) in castrate-resistant, non-metastatic prostate cancer. Am.J.Transl.R
  10. Jellinck, P. H., Forkert, P. G., Riddick, D. S., Okey, A. B., Michnovicz, J. J., and Bradlow, H. L. Ah receptor binding properties of indole carbinols and induction of hepatic estradiol hydroxylation. Biochem.Pharmacol. 3-9-1993;45(5):1129-1136. PubMed
  11. Bui PV, Moualla M, Upson DJ. A Possible Association of Diindolylmethane with Pulmonary Embolism and Deep Venous Thrombosis. Case Rep Med. 2016;2016:7527098. PubMed
  12. Castañon A, Tristram A, Mesher D, Powell N, Beer H, Ashman S, Rieck G, Fielder H, Fiander A, Sasieni P. Effect of diindolylmethane supplementation on low-grade cervical cytological abnormalities: double-blind, randomised, controlled trial. Br J Cancer. 20 PubMed
  13. Le TM, Sanders CJ, van de Corput L, van Erpecum KJ, Röckmann H. Drug rash with eosinophilia and systemic symptoms caused by the dietary supplement diindolylmethane. J Allergy Clin Immunol Pract. 2016 Jan-Feb;4(1):175-6. PubMed
  14. Pence ST, Mehta K, Crum-Bailey J. The Serious Side of Supplements: An Ischemic Stroke in a Healthy 38-year-old Female. Mil Med 2022. PubMed

See these in context on the Diindolylmethane monograph →

Stinging Nettle 23 references
  1. Monographs on the medicinal uses of plant drugs. Exeter, UK: European Scientific Co-op Phytother, 1997.
  2. Newall CA, Anderson LA, Philpson JD. Herbal Medicine: A Guide for Healthcare Professionals. London, UK: The Pharmaceutical Press, 1996.
  3. The Review of Natural Products by Facts and Comparisons. St. Louis, MO: Wolters Kluwer Co., 1999.
  4. Schulz V, Hansel R, Tyler VE. Rational Phytotherapy: A Physician's Guide to Herbal Medicine. Terry C. Telger, transl. 3rd ed. Berlin, GER: Springer, 1998.
  5. Leung AY, Foster S. Encyclopedia of Common Natural Ingredients Used in Food, Drugs and Cosmetics. 2nd ed. New York, NY: John Wiley & Sons, 1996.
  6. Brinker F. Herb Contraindications and Drug Interactions. 2nd ed. Sandy, OR: Eclectic Medical Publications, 1998.
  7. Mittman P. Randomized, double-blind study of freeze-dried Urtica dioica in the treatment of allergic rhinitis. Planta Med 1990;56:44-7.
  8. Vontobel HP, Herzog R, Rutishauser G, Kres H. [Results of a double-blind study on the effectiveness of ERU (extractum radicis Urticae) capsules in conservative treatment of benign prostatic hyperplasia]. (Abstract). Urologe A 1985;24:49-51.
  9. Randall C, Randall H, Dobbs F, et al. Randomized controlled trial of nettle sting for treatment of base-of-thumb pain. J R Soc Med 2000;93:305-9. PubMed
  10. Caliskaner Z, Karaayvaz M, Ozturk S. Misuse of a herb: stinging nettle (Urtica urens) induced severe tongue oedema. Complement Ther Med 2004;12:57-8. PubMed
  11. Krzeski, T., Kazon, M., Borkowski, A., Witeska, A., and Kuczera, J. Combined extracts of Urtica dioica and Pygeum africanum in the treatment of benign prostatic hyperplasia: double-blind comparison of two doses. Clin Ther 1993;15(6):1011-1020.
  12. Randall, C., Meethan, K., Randall, H., and Dobbs, F. Nettle sting of Urtica dioica for joint pain--an exploratory study of this complementary therapy. Complement Ther Med 1999;7(3):126-131. PubMed
  13. Tahri, A., Yamani, S., Legssyer, A., Aziz, M., Mekhfi, H., Bnouham, M., and Ziyyat, A. Acute diuretic, natriuretic and hypotensive effects of a continuous perfusion of aqueous extract of Urtica dioica in the rat. J Ethnopharmacol 2000;73(1-2):95-100. PubMed
  14. Sahin, M., Yilmaz, H., Gursoy, A., Demirel, A. N., Tutuncu, N. B., and Guvener, N. D. Gynaecomastia in a man and hyperoestrogenism in a woman due to ingestion of nettle (Urtica dioica). N.Z.Med.J. 2007;120(1265):U2803.
  15. Randall, C., Dickens, A., White, A., Sanders, H., Fox, M., and Campbell, J. Nettle sting for chronic knee pain: a randomised controlled pilot study. Complement Ther.Med. 2008;16(2):66-72. PubMed
  16. Rayburn, K., Fleischbein, E., Song, J., Allen, B., Kundert, M., Leiter, C., and Bush, T. Stinging nettle cream for osteoarthritis. Altern.Ther.Health Med. 2009;15(4):60-61.
  17. Oliver, F., Amon, E. U., Breathnach, A., Francis, D. M., Sarathchandra, P., Black, A. K., and Greaves, M. W. Contact urticaria due to the common stinging nettle (Urtica dioica)-- histological, ultrastructural and pharmacological studies. Clin Exp Dermato PubMed
  18. Kulze, A. and Greaves, M. Contact urticaria caused by stinging nettles. Br.J Dermatol. 1988;119(2):269-270. PubMed
  19. Patten G. Medicinal plant review: Urtica. Aust J Med Herbalism 1993;5(1):5-13.
  20. Maor D, Little M. Skin contact with a stinging tree requiring intensive care unit admission. Contact Dermatitis. 2017 Nov;77(5):335-37. PubMed
  21. Easton L, Vaid S, Nagel AK, Venci JV, Fortuna RJ. Stinging Nettle (Urtica dioica): An Unusual Case of Galactorrhea. Am J Case Rep 2021;22:e933999. PubMed
  22. Niazi B, Ahmed K, Ahmed M, Ali S, Song K, Elias S. Drug-Induced Liver Injury from Herbal Liver Detoxification Tea. Case Rep Gastroenterol 2022;16(3):612-617. PubMed
  23. Nnamani I, Tolu-Akinnawo O, Dufera RR, Akintunde A, Maliakkal B. Tinospora cordifolia (Guduchi/Giloy)-Induced Liver Injury: A Case Review. Cureus 2023;15(5):e39793. PubMed

See these in context on the Stinging Nettle monograph →

Black Pepper 29 references
  1. Leung AY, Foster S. Encyclopedia of Common Natural Ingredients Used in Food, Drugs and Cosmetics. 2nd ed. New York, NY: John Wiley & Sons, 1996.
  2. Brinker F. Herb Contraindications and Drug Interactions. 2nd ed. Sandy, OR: Eclectic Medical Publications, 1998.
  3. Bano G, Amla V, Raina RK, et al. The effect of piperine on pharmacokinetics of phenytoin in healthy volunteers. Planta Med 1987;53:568-9. PubMed
  4. Bano G, et al. Effect of piperine on bioavailability and pharmacokinetics of propranolol and theophylline in healthy volunteers. Eur J Clin Pharmacol 1991;41;615-7. PubMed
  5. Cohle SD, Trestrail JD III, Graham MA, et al. Fatal pepper aspiration. Am J Dis Child 1988;142:633-6. PubMed
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DISCLAIMER: Currently this does not check for drug-drug interactions. This is not an all-inclusive comprehensive list of potential interactions and is for informational purposes only. Not all interactions are known or well-reported in the scientific literature, and new interactions are continually being reported. Input is needed from a qualified healthcare provider including a pharmacist before starting any therapy. Application of clinical judgment is necessary.

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