Core Ginkgo Blend Ingredients & Drug Interactions
by Energetix
What is this page for?
First and foremost: checking Core Ginkgo Blend 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
Core Ginkgo Blend is a dietary supplement by Energetix with 8 active ingredients. Its ingredients are commonly taken for boosting energy and fighting fatigue, improving mental focus and memory, coping with stress (adaptogen).Based on those ingredients, 1,702 medications have a known interaction with it, the most serious rated major. The ingredients most likely to interact are Ginkgo Leaf Extract, St. John's Wort aerial parts extract, Asian Ginseng Root Extract. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.
Check Your Meds Against Core Ginkgo Blend by Energetix
Ask about any prescription or over-the-counter medication and we check it for interactions with Core Ginkgo Blend by Energetix — and tell you which ingredient is responsible.
AI summaries are generated from our interaction database for education only — always confirm with your pharmacist. How we use AI
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HelloPharmacist Scorecard of Core Ginkgo Blend by Energetix
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.
What’s inside
Low disclosure
Core Ginkgo Blend contains eight active ingredients. The main ones are St.
John's Wort (aerial parts extract), Gotu Kola (aerial parts extract), Ginger Root Extract, Rosemary (aerial parts extract), Ginkgo Leaf Extract, Asian Ginseng Root Extract, and Cayenne Fruit Extract. The product also includes a Botanical Extract Blend and Prickly Ash Bark Extract, along with water, purified water, and ethyl alcohol as inactive ingredients.
Does it work?
Moderate evidence
St. John's Wort is likely effective for depression and possibly effective for somatic symptom disorder and menopausal symptoms, though possibly ineffective for HIV/AIDS and irritable bowel syndrome.
Ginkgo is possibly effective for hearing loss, stroke, schizophrenia, premenstrual syndrome, dementia, and anxiety. Ginger is possibly effective for pregnancy-induced nausea, dysmenorrhea (period pain), and osteoarthritis but possibly ineffective for exercise-induced muscle soreness and chemotherapy-induced nausea.
Gotu Kola is possibly effective for venous insufficiency and burns but possibly ineffective for radiation dermatitis and cognitive function, with insufficient evidence for Alzheimer disease and generalized anxiety. Rosemary is possibly effective for memory, with insufficient evidence for age-related cognitive decline, alopecia, and fatty liver disease.
How safe is it?
Well-documented data
St. John's Wort is generally well tolerated short-term but carries serious risks — it can cause sun sensitivity, diarrhea, dizziness, dry mouth, fatigue, headache, insomnia, and restlessness.
Rare cases of suicidal thoughts and psychosis have been reported. It can trigger mania or hypomania in people with mood disorders and should be avoided during pregnancy and breastfeeding.
Gotu Kola is generally well tolerated but concerns about liver toxicity have been reported in rare cases; it commonly causes nausea and gastric irritation and should be avoided during pregnancy and breastfeeding. Ginger is generally well tolerated but doses above 5 grams daily increase side effects; common ones include stomach discomfort, burping, diarrhea, and heartburn.
Small bowel obstruction is rare. Rosemary is safe in culinary amounts but concentrated forms can cause allergic reactions, lip/gum swelling, occupational asthma, and photosensitivity; medicinal doses should be avoided during pregnancy and breastfeeding.
Ginkgo is generally well tolerated but may increase bleeding risk and rarely causes arrhythmias or spontaneous bleeding; it should be avoided during pregnancy and breastfeeding.
Meds to double-check
Major interaction found
Check your medications carefully if you take digoxin, phenobarbital, phenytoin, mephenytoin, irinotecan, protease inhibitors (HIV drugs), tacrolimus, or docetaxel — St. John's Wort severely reduces their effectiveness.
Also watch for talinolol (a beta-blocker affected by Ginkgo), blood thinners like warfarin, antiplatelet drugs like aspirin, diabetes medications, simvastatin, alprazolam, trazodone, efavirenz, rosiglitazone, and nifedipine. If you take any of these, ask your pharmacist before using this product.
The bottom line
Scorecard at a glanceFormula with limited ingredient disclosure with some supporting evidence for its stated purpose. Major medication interactions have been identified, and safety information is well characterized.
This blend targets memory, cognitive function, and overall vitality — a reasonable choice if those are your goals. However, if you take any prescription medications, especially heart drugs, blood thinners, seizure or diabetes medications, antiretrovirals, or immunosuppressants, you must check each one against the interaction tool before starting.
St. John's Wort and Ginkgo carry significant risks with many common drugs.
Talk to your pharmacist before adding this to your routine.
Educational only — not medical advice; always confirm with your pharmacist. Our editorial policy · How we use AI
Assessment coverage: 7 of 8 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated Aug 22, 2025.
This Scorecard evaluates available label information, ingredient evidence, and known medication-safety considerations. It does not independently verify product identity, purity, potency, contamination, or manufacturing quality. How these ratings are computed
General information
Key facts about Core Ginkgo Blend, straight from the product 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 Core Ginkgo Blend by Energetix, sourced from the NIH Dietary Supplement Label Database.
Supplement Facts
| Ingredient | Amount | % DV |
|---|---|---|
| Asian Ginseng Root Extract | 0 NP | -- |
| St. John's Wort aerial parts extract | 0 NP | -- |
| Gotu Kola Aerial Parts Extract | 0 NP | -- |
| Botanical Extract Blend | 1.2 mL | -- |
| Ginger Root Extract | 0 NP | -- |
| Rosemary Aerial Parts Extract | 0 NP | -- |
| Cayenne Fruit Extract | 0 NP | -- |
| Ginkgo Leaf Extract | 0 NP | -- |
| Prickly Ash Bark Extract | 0 NP | -- |
Other ingredients: Water, Purified, Ethyl Alcohol
Tap any ingredient to jump to its full detail below.
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.
Suggested/Recommended/Usage/Directions
As a dietary supplement, take 30 to 40 drops orally (in water or juice, if desired) twice daily or as directed by a healthcare professional. Shake well before use.
Precautions
Do not use if neck wrap is broken or missing.
If pregnant or breast-feeding, ask a healthcare professional before use.
Keep out of reach of children.
Storage
Store at room temperature out of direct sunlight.
FDA Statement of Identity
Dietary Supplement
Formulation
Spagyrically processed botanical
Is this label outdated? Report a formula or label change and our pharmacy team will review it.
Core Ginkgo Blend by Energetix label
The label scan from the NIH Dietary Supplement Label Database. Tap to enlarge.
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)The Ingredients in Core Ginkgo Blend by Energetix
These are the 8 active ingredients this product is made of. Select any to open its full monograph.
Serving size1.2 mL Dosage formLiquid Servings per container49 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.
Botanical Extract Blend
Other (inactive) ingredients: Water, Purified, Ethyl Alcohol. These complete the product’s ingredient list but are not active constituents.
Core Ginkgo Blend by Energetix Drug Interactions
HelloPharmacist Interaction Report
Energetix Core Ginkgo Blend contains several ingredients with documented interactions, and the most serious concerns involve St.
John's Wort, which carries Major-severity interactions with multiple medications. St.
John's Wort significantly reduces blood levels of digoxin (a heart medication), phenobarbital and phenytoin (seizure drugs), mephenytoin (another seizure drug), irinotecan (a cancer drug), protease inhibitors used for HIV, tacrolimus (an immunosuppressant), and docetaxel (a cancer drug) — meaning these medications become less effective when taken together.
Read the full breakdown — every affected drug type, severity by severity
Ginkgo leaf extract has its own Major interaction with talinolol (a beta-blocker), which increases that drug's blood levels and raises the risk of side effects. The product also contains Ginger, Rosemary, and Gotu Kola, each with Moderate interactions affecting blood thinners (anticoagulants and antiplatelets like warfarin), diabetes medications, some heart drugs, and other medication classes.
Ginkgo adds Moderate interactions with simvastatin (a statin), alprazolam (an anxiety drug), warfarin, trazodone (an antidepressant), efavirenz (an HIV medication), rosiglitazone (a diabetes drug), and tacrolimus.
We could not check three ingredients — Asian Ginseng Root Extract, Cayenne Fruit Extract, and Prickly Ash Bark Extract — because we hold no interaction data for them. Altogether, these interactions span 1,550 individual medications.
Before you start this product, search for each of your current medications using the tool on this page to see if any are affected.
Check your own medications below · Editorial policy · How we use AI
Want to check YOUR meds against Core Ginkgo Blend?
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 checkerIngredients driving the most interactions
Individual Drug Interactions
The ingredients in Core Ginkgo Blend interact with 1,702 drugs. Click any drug to see the details.
7 of the 8 ingredients in Core Ginkgo Blend interact with drugs. Each result below shows which ingredient is responsible. Ginkgo Leaf Extract St. John's Wort aerial parts extract Asian Ginseng Root Extract Ginger Root Extract Gotu Kola Aerial Parts Extract Rosemary Aerial Parts Extract Prickly Ash Bark Extract
Alginic Acid, Aluminum HydroxideRafton
How Alginic Acid, Aluminum Hydroxide interacts with Core Ginkgo Blend — through 1 ingredient. Tap an ingredient for the detail:
Prickly Ash Bark ExtractAntacids Minor
Interaction Summary
Theoretically, northern prickly ash might decrease the effectiveness of antacids.
Read the full Prickly Ash Bark Extract + Alginic Acid, Aluminum Hydroxide interactionAluminum HydroxideAlu-Cap, Amphojel, Gaviscon
How Aluminum Hydroxide interacts with Core Ginkgo Blend — through 1 ingredient. Tap an ingredient for the detail:
Prickly Ash Bark ExtractAntacids Minor
Interaction Summary
Theoretically, northern prickly ash might decrease the effectiveness of antacids.
Read the full Prickly Ash Bark Extract + Aluminum Hydroxide interactionAluminum Hydroxide, Magnesium Hydroxide (otc Drug)Maalox, Mucogel
How Aluminum Hydroxide, Magnesium Hydroxide (otc Drug) interacts with Core Ginkgo Blend — through 1 ingredient. Tap an ingredient for the detail:
Prickly Ash Bark ExtractAntacids Minor
Interaction Summary
Theoretically, northern prickly ash might decrease the effectiveness of antacids.
Read the full Prickly Ash Bark Extract + Aluminum Hydroxide, Magnesium Hydroxide (otc Drug) interactionAluminum Hydroxide, Magnesium Hydroxide, Simethicone (otc Drug)Mylanta
How Aluminum Hydroxide, Magnesium Hydroxide, Simethicone (otc Drug) interacts with Core Ginkgo Blend — through 1 ingredient. Tap an ingredient for the detail:
Prickly Ash Bark ExtractAntacids Minor
Interaction Summary
Theoretically, northern prickly ash might decrease the effectiveness of antacids.
Read the full Prickly Ash Bark Extract + Aluminum Hydroxide, Magnesium Hydroxide, Simethicone (otc Drug) interactionAluminum, Magnesium (otc Drug)Almagel
How Aluminum, Magnesium (otc Drug) interacts with Core Ginkgo Blend — through 1 ingredient. Tap an ingredient for the detail:
Prickly Ash Bark ExtractAntacids Minor
Interaction Summary
Theoretically, northern prickly ash might decrease the effectiveness of antacids.
Read the full Prickly Ash Bark Extract + Aluminum, Magnesium (otc Drug) interactionBismuth Subcarbonate, Calcium Carbonate, OpiumDiabismul
How Bismuth Subcarbonate, Calcium Carbonate, Opium interacts with Core Ginkgo Blend — through 1 ingredient. Tap an ingredient for the detail:
Prickly Ash Bark ExtractAntacids Minor
Interaction Summary
Theoretically, northern prickly ash might decrease the effectiveness of antacids.
Read the full Prickly Ash Bark Extract + Bismuth Subcarbonate, Calcium Carbonate, Opium interactionCalcium CarbonateAdcal, Adcal-D3, Calcichew, Os-Cal, Tums
How Calcium Carbonate interacts with Core Ginkgo Blend — through 1 ingredient. Tap an ingredient for the detail:
Prickly Ash Bark ExtractAntacids Minor
Interaction Summary
Theoretically, northern prickly ash might decrease the effectiveness of antacids.
Read the full Prickly Ash Bark Extract + Calcium Carbonate interactionDihydroxyaluminum Sodium CarbonateRolaids
How Dihydroxyaluminum Sodium Carbonate interacts with Core Ginkgo Blend — through 1 ingredient. Tap an ingredient for the detail:
Prickly Ash Bark ExtractAntacids Minor
Interaction Summary
Theoretically, northern prickly ash might decrease the effectiveness of antacids.
Read the full Prickly Ash Bark Extract + Dihydroxyaluminum Sodium Carbonate interactionMagaldrateRiopan
How Magaldrate interacts with Core Ginkgo Blend — through 1 ingredient. Tap an ingredient for the detail:
Prickly Ash Bark ExtractAntacids Minor
Interaction Summary
Theoretically, northern prickly ash might decrease the effectiveness of antacids.
Read the full Prickly Ash Bark Extract + Magaldrate interactionNizatidineAxid, Axid Injection
How Nizatidine interacts with Core Ginkgo Blend — through 1 ingredient. Tap an ingredient for the detail:
Prickly Ash Bark ExtractH2-blockers Minor
Interaction Summary
Theoretically, northern prickly ash might decrease the effectiveness of H2-blockers.
Read the full Prickly Ash Bark Extract + Nizatidine interactionSodium Bicarbonate (otc Drug)Sodium Bicarbonate
How Sodium Bicarbonate (otc Drug) interacts with Core Ginkgo Blend — through 1 ingredient. Tap an ingredient for the detail:
Prickly Ash Bark ExtractAntacids Minor
Interaction Summary
Theoretically, northern prickly ash might decrease the effectiveness of antacids.
Read the full Prickly Ash Bark Extract + Sodium Bicarbonate (otc Drug) interactionEach ingredient & the kinds of drugs it affects
For each ingredient in Core Ginkgo Blend 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 Leaf Extract
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.
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.
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.
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.
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.
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.
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.
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.
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.
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).
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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%.
St. John's Wort aerial parts extract
Alprazolam (Xanax)
St. John's wort increases the clearance of alprazolam and decreases its effects.
Alprazolam, which is used as a probe for cytochrome P450 3A4 (CYP3A4) activity, has a two-fold increase in clearance when given with St. John's wort. St. John's wort reduces the half-life of alprazolam from 12.4 hours to 6 hours.
Contraceptive Drugs
St. John's wort increases the clearance of contraceptive drugs and reduces their clinical effects.
Females taking St. John's wort and oral contraceptives concurrently should use an additional or alternative form of birth control. St. John's wort can decrease norethindrone and ethinyl estradiol levels by 13% to 15%, resulting in breakthrough bleeding, irregular menstrual bleeding, or unplanned pregnancy. Bleeding irregularities usually occur within a week of starting St. John's wort and regular cycles usually return when St. John's wort is discontinued. Unplanned pregnancy has occurred with concurrent use of oral contraceptives and St. John's wort extract. St. John's wort is thought to induce the cytochrome P450 1A2 (CYP1A2), 2C9 (CYP2C9), and 3A4 (CYP3A4) enzymes, which are responsible for metabolism of progestins and estrogens in contraceptives.
Cyclosporine (Neoral, Sandimmune)
St. John's wort reduces the levels and clinical effects of cyclosporine.
Concomitant use can decrease plasma cyclosporine levels by 30% to 70%. Using St. John's wort with cyclosporine in patients with heart, kidney, or liver transplants can cause subtherapeutic cyclosporine levels and acute transplant rejection. This interaction has occurred with a St. John's wort extract standardized to 0.3% hypericin and dosed at 300-600 mg per day. Withdrawal of St. John's wort can result in a 64% increase in cyclosporine levels. St. John's wort induces cytochrome P450 3A4 (CYP3A4) and the multi-drug transporter, P-glycoprotein/MDR-1, which increases cyclosporine clearance.
Cytochrome P450 3A4 (Cyp3A4) Substrates
St. John's wort increases the metabolism and reduces the levels of CYP3A4 substrates.
St. John's wort induces CYP3A4 enzymes and increases metabolism of CYP3A4 substrates. Clinically significant interactions have been reported with St. John's wort products containing hyperforin 1 mg or more.
Digoxin (Lanoxin)
St. John's wort reduces the levels and clinical effects of digoxin.
St. John's wort can reduce the bioavailability, serum levels, and therapeutic effects of digoxin. Taking an extract of St. John's wort 900 mg, containing hyperforin 7.5 mg or more, daily for 10-14 days, can reduce serum digoxin levels by 25% in healthy people. St. John's wort is thought to affect the multidrug transporter, P-glycoprotein, which mediates the absorption and elimination of digoxin and other drugs. St. John's wort products providing less than 7.5 mg of hyperforin daily do not appear to affect digoxin levels.
Docetaxel (Taxotere)
St. John's wort reduces the levels and clinical effects of docetaxel.
Clinical research shows that taking a specific St. John's wort product (Hyperiplant, VSM) 300 mg three times daily for 14 days increases docetaxel clearance by about 14%, resulting in decreased plasma concentrations of docetaxel in cancer patients. This is most likely due to induction of cytochrome P450 3A4 (CYP3A4) by St. John's wort.
Imatinib (Gleevec)
St. John's wort reduces the levels and clinical effects of imatinib.
Taking St. John's wort 900 mg daily for 2 weeks reduces the bioavailability and half-life of a single dose of imatinib and decreases its serum levels by 30% in healthy volunteers. This is most likely due to induction of cytochrome P450 3A4 (CYP3A4) by St. John's wort, which increases clearance of imatinib.
Irinotecan (Camptosar)
St. John's wort reduces the levels and clinical effects of irinotecan.
St. John's wort 900 mg daily for 18 days decreases serum levels of irinotecan by at least 50%. Clearance of the active metabolite of irinotecan, SN-38, is also increased, resulting in a 42% decrease in the area under the concentration-time curve. This is thought to be due to induction of cytochrome P450 3A4 (CYP3A4) by St. John's wort.
Mephenytoin (Mesantoin)
St. John's wort reduces the levels and clinical effects of mephenytoin.
Preliminary clinical research in healthy males shows that taking St. John's wort for 14 days induces cytochrome P450 2C19 (CYP2C19) and significantly increases metabolism of mephenytoin (Mesantoin). In people with wild-type 2C19, metabolism was almost 4-fold greater in subjects who received St. John's wort compared to placebo. In contrast, patients with 2C19*2/*2 and *2/*3 genotypes did not demonstrate a similar increase in metabolism.
Non-Nucleoside Reverse Transcriptase Inhibitors (Nnrtis)
St. John's wort decreases the levels and clinical effects of NNRTIs.
St. John's wort increases the oral clearance of nevirapine (Viramune) by 35%. Subtherapeutic concentrations are associated with therapeutic failure, development of viral resistance, and development of drug class resistance. St. John's wort induces intestinal and hepatic cytochrome P450 3A4 (CYP3A4) and intestinal P-glycoprotein/MDR-1, a drug transporter.
Omeprazole (Prilosec)
St. John's wort decreases the levels and clinical effects of omeprazole.
Taking St. John's wort, 300 mg orally three times daily for 14 days, reduces serum concentrations of omeprazole by inducing its metabolism via cytochrome P450 (CYP) 2C19 and 3A4. The reduction of omeprazole serum levels is dependent on CYP2C19 genotype, with reductions up to 50% in extensive metabolizers and 38% in poor metabolizers.
Oxycodone (Oxycontin)
St. John's wort decreases the levels and clinical effects of oxycodone.
St. John's wort can increase oxycodone metabolism by inducing cytochrome P450 3A4 (CYP3A4), reducing plasma levels and analgesic activity.
P-Glycoprotein Substrates
St. John's wort decreases the levels and clinical effects of P-glycoprotein substrates.
St. John's wort induces P-glycoprotein. P-glycoprotein is a carrier mechanism responsible for transporting drugs and other substances across cell membranes. When P-glycoprotein is induced in the gastrointestinal (GI) tract, it can prevent the absorption of some medications. In addition, induction of p-glycoprotein can decrease entry of drugs into the central nervous system (CNS) and decrease access to other sites of action.
Phenobarbital (Luminal)
St. John's wort decreases the levels and clinical effects of phenobarbital.
St. John's wort may increase the metabolism of phenobarbital. Plasma concentrations of phenobarbital should be monitored carefully. The dose of phenobarbital may need to be increased when St. John's wort is started and decreased when it is stopped.
Phenprocoumon (Marcoumar, Others)
St. John's wort decreases the levels and clinical effects of phenprocoumon.
St. John's wort appears to increase the metabolism of phenprocoumon (an anticoagulant that is not available in the US) by increasing the activity of the cytochrome P450 2C9 (CYP2C9) enzyme. This may result in decreases in the anticoagulant effect and international normalized ratio (INR).
Phenytoin (Dilantin)
St. John's wort decreases the levels and clinical effects of phenytoin.
St. John's wort may increase the metabolism of phenytoin. Plasma concentrations of phenytoin should be monitored closely. The dose of phenytoin may need to be increased when St. John's wort is started and decreased when it is stopped.
Protease Inhibitors (Pis)
St. John's wort reduces the levels and clinical effects of PIs.
In healthy volunteers, St. John's wort can reduce the plasma concentrations of indinavir (Crixivan) by inducing cytochrome P450 3A4 (CYP3A4). This might result in treatment failure and viral resistance. St. John's wort also induces P-glycoprotein, which can result in decreased intracellular protease inhibitor concentrations and increased elimination.
Rivaroxaban (Xarelto)
St. John's wort decreases the levels and clinical effects of rivaroxaban.
A small pharmacokinetic study in healthy volunteers shows that taking a single dose of rivaroxaban 20 mg after using a specific St. John's wort extract (Jarsin, Vifor SA) 450 mg orally twice daily for 14 days reduces the bioavailability of rivaroxaban by 24% and reduces rivaroxaban's therapeutic inhibition of factor Xa by 20%.
Tacrolimus (Prograf)
St. John's wort decreases the levels and clinical effects of tacrolimus.
Taking a St. John's wort extract (Jarsin) 600 mg daily significantly decreases tacrolimus serum levels. Dose increases of 60% may be required to maintain therapeutic tacrolimus levels in patients taking St. John's wort. St. John's wort is thought to lower tacrolimus levels by inducing cytochrome P450 3A4 (CYP3A4) enzymes. A small clinical study in healthy adults also shows that taking St. John's wort 300 mg three times daily for 10 days decreases the total systemic exposure to tacrolimus by 27% and 33% after taking a single 5 mg dose of immediate-release or prolonged-release tacrolimus, respectively.
Warfarin (Coumadin)
St. John's wort decreases the levels and clinical effects of warfarin.
Taking St. John's wort significantly increases clearance of warfarin, including both its R- and S-isomers. This is likely due to induction of cytochrome P450 (CYP) 1A2 and CYP3A4. St. John's wort can also significantly decrease International Normalized Ratio (INR) in people taking warfarin. In addition, taking warfarin at the same time as St. John's wort might reduce warfarin bioavailability. When a dried extract is mixed with warfarin in an aqueous medium, up to 30% of warfarin is bound to particles, reducing its absorption.
Aminolevulinic Acid
St. John's wort might have additive phototoxic effects with aminolevulinic acid.
Concomitant use with St. John's wort extract may cause synergistic phototoxicity. Delta-aminolevulinic acid can cause a burning erythematous rash and severe swelling of the face, neck, and hands when taken with St. John's wort.
Bupropion (Wellbutrin)
St. John's wort might reduce the levels and effects of bupropion.
Clinical research shows that taking St. John's wort 325 mg three times daily for 14 days along with bupropion reduces the area under the concentration-time curve by approximately 14% and increases the clearance of bupropion by approximately 20%. This effect is attributed to the induction of cytochrome P450 2B6 (CYP2B6) by St. John's wort.
Clopidogrel (Plavix)
St. John's wort might increase the levels and effects of clopidogrel.
Taking St. John's wort with clopidogrel seems to increase the activity of clopidogrel. In clopidogrel non-responders, taking St. John's wort seems to induce metabolism of clopidogrel to its active metabolite by cytochrome P450 enzymes 3A4 and 2C19. This leads to increased antiplatelet activity. Theoretically, this might lead to an increased risk of bleeding in clopidogrel responders.
Clozapine (Clozaril)
St. John's wort might decrease the levels and clinical effects of clozapine.
A case report describes a female with schizophrenia controlled on clozapine who had a return of symptoms when she started taking St. John's wort. The plasma concentration of clozapine was reduced, likely because its clearance was increased due to induction of the cytochrome P450 enzymes 3A4, 1A2, 2C9, and 2C19 by St. John's wort.
Cytochrome P450 1A2 (Cyp1A2) Substrates
St. John's wort may increase the metabolism and reduce the levels of CYP1A2 substrates.
Clinical and in vitro research shows that St. John's wort induces CYP1A2, but to a lesser extent than CYP3A4.
Asian Ginseng Root Extract
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.
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.
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.
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.
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.
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.
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.
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.
Immunosuppressants
Theoretically, Panax ginseng use might interfere with immunosuppressive therapy.
Panax ginseng might have immune system stimulating properties.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Ginger Root Extract
Anticoagulant/Antiplatelet Drugs
Ginger may have antiplatelet effects and may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs. However, research is conflicting.
Laboratory research suggests that ginger inhibits thromboxane synthetase and decreases platelet aggregation. However, this has not been demonstrated unequivocally in humans, with mixed results from clinical trials. Theoretically, excessive amounts of ginger might increase the risk of bleeding when used with anticoagulant/antiplatelet drugs.
Antidiabetes Drugs
Theoretically, taking ginger with antidiabetes drugs might increase the risk of hypoglycemia.
Animal and human research suggests that ginger might increase insulin levels and/or decrease blood glucose levels.
Cytochrome P450 3A4 (Cyp3A4) Substrates
Ginger might increase or decrease the levels of CYP3A4 substrates.
In vitro research and some case reports suggest that ginger inhibits CYP3A4 activity. Three case reports from the World Health Organization (WHO) adverse drug reaction database describe increased toxicity in patients taking ginger and cancer medications that are CYP3A4 substrates (imatinib, dabrafenib, and crizotinib). However, the causality of this interaction is unclear due to the presence of multiple interacting drugs and routes of administration.
Conversely, other in vitro research suggests that ginger induces CYP3A4 activity, leading to reduced levels of CYP3A4 substrates. However, this interaction has not been reported in humans.
Losartan (Cozaar)
Theoretically, ginger might increase levels of losartan and the risk of hypotension.
In animal research, ginger increased the levels and hypotensive effects of a single dose of losartan. It is not clear if ginger alters the concentration or effects of losartan when taken continuously. Additionally, this interaction has not been shown in humans.
Nifedipine (Procardia)
Ginger may have antiplatelet effects and increase the risk of bleeding if used with nifedipine.
Clinical research shows that combined treatment with ginger 1 gram plus nifedipine 10 mg significantly inhibits platelet aggregation when compared to nifedipine or ginger alone.
P-Glycoprotein Substrates
Ginger might increase the absorption and blood levels of P-glycoprotein (P-gp) substrates.
In vitro research and case reports suggest that ginger inhibits drug efflux by P-gp, potentially increasing absorption and serum levels of P-gp substrates. Two case reports from the World Health Organization (WHO) adverse drug reaction database describe increased toxicity in patients taking ginger and cancer medications that are P-gp substrates (trametinib, crizotinib). However, the causality of this interaction is unclear due to the presence of multiple interacting drugs and routes of administration.
Phenprocoumon (Marcoumar, Others)
Ginger might increase the risk of bleeding with phenprocoumon.
Phenprocoumon, a warfarin-related anticoagulant, might increase the international normalized ratio (INR) when taken with ginger. There is one case report of a 76-year-old woman with a stable INR on phenprocoumon that increased to greater than 10 when she began consuming dried ginger and ginger tea.
Warfarin (Coumadin)
Ginger might increase the risk of bleeding with warfarin.
Laboratory research suggests that ginger might inhibit thromboxane synthetase and decrease platelet aggregation. In one case report, ginger increased the INR when taken with phenprocoumon, which has similar pharmacological effects as warfarin. In another case report, ginger increased the INR when taken with a combination of warfarin, hydrochlorothiazide, and acetaminophen. A longitudinal analysis suggests that taking ginger increases the risk of bleeding in patients taking warfarin for at least 4 months. However, research in healthy people suggests that ginger has no effect on INR, or the pharmacokinetics or pharmacodynamics of warfarin. Until more is known, monitor INRs closely in patients taking large amounts of ginger.
Calcium Channel Blockers
Theoretically, taking ginger with calcium channel blockers might increase the risk of hypotension.
Some animal and in vitro research suggests that ginger has hypotensive and calcium channel-blocking effects. Another animal study shows that concomitant administration of ginger and the calcium channel blocker amlodipine leads to greater reductions in blood pressure when compared with amlodipine alone.
Cyclosporine (Neoral, Sandimmune)
Theoretically, when taken prior to cyclosporine, ginger might decrease cyclosporine levels.
In an animal model, ginger juice taken 2 hours prior to cyclosporine administration reduced the maximum concentration and area under the curve of cyclosporine by 51% and 40%, respectively. This effect was not observed when ginger juice and cyclosporine were administered at the same time.
Cytochrome P450 1A2 (Cyp1A2) Substrates
Theoretically, ginger might increase the levels of CYP1A2 substrates.
In vitro research shows that ginger inhibits CYP1A2 activity. However, this interaction has not been reported in humans.
Cytochrome P450 2B6 (Cyp2B6) Substrates
Theoretically, ginger might increase the levels of CYP2B6 substrates.
In vitro research shows that ginger inhibits CYP2B6 activity. However, this interaction has not been reported in humans.
Cytochrome P450 2C9 (Cyp2C9) Substrates
Theoretically, ginger might increase the levels of CYP2C9 substrates.
In vitro research shows that ginger inhibits CYP2C9 activity. However, this interaction has not been reported in humans.
Metronidazole (Flagyl)
Theoretically, ginger might increase levels of metronidazole.
In an animal model, ginger increased the absorption and plasma half-life of metronidazole. In addition, the elimination rate and clearance of metronidazole was significantly reduced.
Gotu Kola Aerial Parts Extract
Cns Depressants
Theoretically, taking gotu kola might increase the sedative effects of CNS depressants.
In vitro research suggests that gotu kola may have sedative effects via binding of GABA receptors.
Hepatotoxic Drugs
Theoretically, taking gotu kola with hepatotoxic drugs might have additive adverse effects.
There are at least four case reports of hepatotoxicity associated with the use of gotu kola. However, more information is needed to determine if gotu kola was the causative factor in these cases.
Rosemary Aerial Parts Extract
Anticoagulant/Antiplatelet Drugs
Theoretically, rosemary may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
In vitro and animal research suggests that rosemary inhibits platelet aggregation.
Antidiabetes Drugs
Theoretically, taking rosemary with antidiabetes drugs might increase the risk of hypoglycemia.
Animal research shows that rosemary extract can decrease blood glucose levels in diabetic models. However, research in humans is conflicting. Although rosemary powder decreased blood glucose levels in healthy adults, no change in blood glucose levels was seen in adults with type 2 diabetes, most of whom were taking antidiabetes drugs.
Aspirin
Theoretically, rosemary might have additive effects with salicylate-containing drugs such as aspirin.
Rosemary is reported to contain salicylates.
Choline Magnesium Trisalicylate (Trilisate)
Theoretically, rosemary might have additive effects with salicylate-containing drugs such as choline magnesium trisalicylate.
Rosemary is reported to contain salicylate.
Salsalate (Disalcid)
Theoretically, rosemary might have additive effects with salicylate-containing drugs such as salsalate.
Rosemary is reported to contain salicylate.
Cytochrome P450 1A2 (Cyp1A2) Substrates
Theoretically, rosemary might decrease the levels and clinical effects of CYP1A2 substrates.
In vitro research shows that rosemary induces CYP1A2 enzymes. This effect has not been reported in humans.
Prickly Ash Bark Extract
Antacids
Theoretically, northern prickly ash might decrease the effectiveness of antacids.
There are reports that northern prickly ash increases stomach acid.
H2-Blockers
Theoretically, northern prickly ash might decrease the effectiveness of H2-blockers.
There are reports that northern prickly ash increases stomach acid.
Proton Pump Inhibitors (Ppis)
Theoretically, northern prickly ash might decrease the effectiveness of PPIs.
There are reports that northern prickly ash increases stomach acid.
Brand information
Manufacturer and brand details for Core Ginkgo Blend, from the product label.
Core Ginkgo Blend by Energetix: Common Questions
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Written and reviewed by the HelloPharmacist editorial staff. Our editorial policy
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The Full Monographs Behind Core Ginkgo Blend’s Ingredients
Every ingredient we hold a full HelloPharmacist monograph for — uses, evidence, safety, and the complete interaction list.
Panax Ginseng
Interacts with 1,130 drugsPanax 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 monographSt. John's Wort
Interacts with 1,143 drugsSt. John's wort is a well-studied herb most often used for mild to moderate depression, and some research suggests it may help with this. However, it has many serious interactions with presc...
Read the full St. John's Wort monograph → Herb & supplement monographGotu Kola
Interacts with 579 drugsGotu kola is a traditional Ayurvedic and Asian herb that people use for wound healing, circulation, skin problems, and as a calming or memory-supporting herb. Some early studies suggest poss...
Read the full Gotu Kola monograph → Herb & supplement monographGinger
Interacts with 1,007 drugsGinger is a widely used culinary spice with a long history in traditional medicine, and it has the strongest evidence for helping with nausea and vomiting, including from motion sickness, pr...
Read the full Ginger monograph → Herb & supplement monographRosemary
Interacts with 372 drugsRosemary is a fragrant Mediterranean herb that is safe and flavorful in normal food amounts. Some early research suggests possible benefits for memory, mood, and hair growth, but the evidenc...
Read the full Rosemary monograph → Herb & supplement monographGinkgo
Interacts with 1,266 drugsGinkgo 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 monographNorthern Prickly Ash
Interacts with 36 drugsNorthern Prickly Ash is a North American shrub whose bark and berries have a long history in folk medicine, especially for toothache, joint pain, and sluggish digestion. Modern scientific ev...
Read the full Northern Prickly Ash monograph →Sources & How We Checked
Core Ginkgo Blend'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.
- NIH Dietary Supplement Label Database (DSLD) — The official product label on file for this supplement.
- Natural Medicines (Therapeutic Research Center) — Evidence-graded clinical reference behind the ingredient interaction data.
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 419 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.
Panax Ginseng 66 references
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- Palmer BV, Montgomery AC, Monteiro JC, et al. Gin Seng and mastalgia [letter]. BMJ 1978;1:1284. PubMed
- Hopkins MP, Androff L, Benninghoff AS. Ginseng face cream and unexplained vaginal bleeding. Am J Obstet Gynecol 1988;159:1121-2. PubMed
- Greenspan EM. Ginseng and vaginal bleeding [letter]. JAMA 1983;249:2018.
- Gonzalez-Seijo JC, Ramos YM, Lastra I. Manic episode and ginseng: Report of a possible case. J Clin Psychopharmacol 1995;15:447-8.
- Dega H, Laporte JL, Frances C, et al. Ginseng as a cause of Stevens-Johnson syndrome. Lancet 1996;347:1344.
- Hamid S, Rojter S, Vierling J. Protracted cholestatic hepatitis after the use of Prostata. Ann Intern Med 1997;127:169-70.
- Shader RI, Greenblatt DJ. Phenelzine and the dream machine-ramblings and reflections. J Clin Psychopharmacol 1985;5:65. PubMed
- Jones BD, Runikis AM. Interaction of ginseng with phenelzine. J Clin Psychopharmacol 1987;7:201-2. PubMed
- Janetzky K, Morreale AP. Probable interaction between warfarin and ginseng. Am J Health Syst Pharm 1997;54:692-3. PubMed
- Becker BN. Ginseng-induced diuretic resistance. JAMA 1996;276:606-7. PubMed
- Gurley BJ, Gardner SF, Hubbard MA. Clinical assessment of potential cytochrome P450-mediated herb-drug interactions. AAPS Ann Mtg & Expo Indianapolis, IN: 2000; Oct 29 - Nov 2:presentation #3460.
- Park HJ, Lee JH, Song YB, Park KH. Effects of dietary supplementation of lipophilic fraction from Panax ginseng on cGMP and cAMP in rat platelets and on blood coagulation. Biol Pharm Bull 1996;19:1434-9. PubMed
- Zhu M, Chan KW, Ng LS, et al. Possible influences of ginseng on the pharmacodynamics of warfarin in rats. J Pharm Pharmacol 1999;51:175-80.
- Choi HK, Jung GW, Moon KH, et al. Clinical study of SS-Cream in patients with lifelong premature ejaculation. Urology 2000;55:257-61. PubMed
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Northern Prickly Ash 2 references
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See these in context on the Northern Prickly Ash monograph →
Parts of this content are provided by the Therapeutic Research Center, LLC.
DISCLAIMER: Currently this does not check for drug-drug interactions. This is not an all-inclusive comprehensive list of potential interactions and is for informational purposes only. Not all interactions are known or well-reported in the scientific literature, and new interactions are continually being reported. Input is needed from a qualified healthcare provider including a pharmacist before starting any therapy. Application of clinical judgment is necessary.
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