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Dietary supplement

Focus Formula Ingredients & Drug Interactions

by Focus Formula

Focus Formula label
See full label image
Tablet Or Pill Category: Other Combinations
Most serious interaction: Major
Clinical methodology reviewed by · Updated Sep 16, 2026 · Label data from the NIH DSLD
What is this page for?

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

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

The interaction bottom line Most serious interaction: Major

Focus Formula is a dietary supplement by Focus Formula with 9 active ingredients. Its ingredients are commonly taken for diabetic nerve pain (neuropathy), blood sugar support in diabetes, antioxidant support.Based on those ingredients, 1,624 medications have a known interaction with it, the most serious rated major. The ingredients most likely to interact are Ginkgo biloba extract, Caffeine, GABA. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.

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Check Your Meds Against Focus Formula by Focus Formula

Ask about any prescription or over-the-counter medication and we check it for interactions with Focus Formula by Focus Formula — and tell you which ingredient is responsible.

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Computed from our clinical databases

HelloPharmacist Scorecard of Focus Formula by Focus Formula

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

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

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

Why this rating?
  • We haven't mapped this product's purpose to our evidence data yet — it'll be graded on the next content refresh.
Ingredient Transparency
Full

Every active ingredient lists its own amount on the label.

Why this rating?
  • The label discloses an exact amount for 9 of its 9 active ingredients.
  • No proprietary blends here — you can verify the dose of every single component.
Known Interaction Concern
Major identified

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

Why this rating?
  • 8 of the 9 matched ingredients can interact with medications — Vinpocetine, Toothed Clubmoss, Ginkgo, Gamma-aminobutyric Acid (gaba), Deanol, among others.
  • The most serious interaction on file is rated Major.
  • Some involve high-stakes drug classes: anticoagulant / antiplatelet drugs; seizure medications; immunosuppressants / transplant drugs; cancer treatments; diabetes medications; lithium.
  • For scale: 1,625 individual medications appear in the full list. A big number alone doesn't make a product dangerous — what matters is whether YOUR medication is on it, so run yours through the interaction checker on this page.
Safety Information
Well characterized

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

Why this rating?
  • We hold adverse-effect (side-effect) data for 9 of the 9 matched ingredients.
  • Pregnancy & breastfeeding safety ratings cover 9 of 9.
  • General safety write-ups exist for 9 of 9.
  • Remember: this measures how much safety information exists. Thin data is not the same as being safe.

HelloPharmacist summaryFully disclosed formula with no assessable stated purpose. Major medication interactions have been identified, and safety information is well characterized.

Assessment coverage: 9 of 9 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated Feb 24, 2017.

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 Focus Formula, straight from the product label.

Brand Focus Formula
Barcode (UPC) 335046098193
Net contents 60 Tablet(s)
Market status Off market
Date entered into DSLD Feb 24, 2017
DSLD ID 71159
Product type Other Combinations
Supplement form Tablet Or Pill
Dietary claims / uses All Other, Structure/Function
Intended target group(s) Adult (18 - 50 Years)
From the label
Everything in this section is reproduced from the manufacturer’s own product label — it’s the label speaking, not HelloPharmacist. We show it so you can see exactly what the maker states; we don’t verify or endorse those statements.

Supplement Facts

The label details for Focus Formula by Focus Formula, 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:
2 Tablet(s)
Maximum serving Sizes:
2 Tablet(s)
Servings per container
30
UPC/BARCODE
335046098193
IngredientAmount% DV
Alpha-Lipoic Acid50 mg--
Vinpocetine2.5 mg--
GABA100 mg--
DMAE (Dimethylaminoethanol) Bitartrate125 mg--
Soy Lecithin200 mg--
Omega-3 Complex15 mg--
Ginkgo biloba extract60 mg--
Caffeine50 mg--
Huperzia serrata extract100 mcg--

Other ingredients: Calcium Carbonate, Microcrystalline Cellulose, Stearic Acid, Croscarmellose Sodium, Coating, Crospovidone, Magnesium Stearate, Silica

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

Contains soy and fish.

Precautions

Contains soy and fish.

Do not exceed recommended intake.

Keep out of reach of children.

Do not use if inner seal is broken.

Warning: Consult a physician before use. Do not use if you have high blood pressure or heart problem, or are contemplating becoming pregnant.

Consult a physician before use if you are pregnant or nursing, or are taking prescription drugs.

Suggested/Recommended/Usage/Directions

Directions: Take 2 tablets daily with a meal, as a dietary supplement or as directed by a healthcare professional.

FDA Disclaimer Statement

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

General Statements

Focus formula may support: Memory Concentration Recall Attention Alertness Mental clarity Blood flow

Clinically proven ingredients

Supports brain in 4 ways! 1 - Improve focus & concentration 2 - Supports memory & recall 3 - Boosts energy & attention 4 - Promotes blood flow

Supports brain health

Storage

Store in a cool, dry place. Protect from heat, light, moisture.

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

See for yourself

Focus Formula by Focus Formula label

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

Focus Formula label

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

View the full label (PDF)
What’s inside

The Ingredients in Focus Formula by Focus Formula

These are the 9 active ingredients this product is made of. Select any to open its full monograph.

Serving size2 Tablet(s) Dosage formTablet Or Pill Servings per container30 Amounts shown are per serving.

Most supplement products combine several ingredients, and a medication can interact with the product through any one of them. Each ingredient below shows whether it has known drug interactions.

Alpha-Lipoic Acid

Interacts with
263 drugs
50 mg per serving

Alpha-lipoic acid (ALA) is an antioxidant made naturally by the body and found in small amounts in foods. It is most studied for diabetic nerve pain,...

Alpha-Lipoic Acid monograph & interactions

Vinpocetine

Interacts with
208 drugs
2.5 mg per serving

Vinpocetine is a lab-made compound based on a chemical from the periwinkle plant, and it is marketed mainly for memory and brain health. The evidence...

Vinpocetine monograph & interactions

GABA

Interacts with
419 drugs
100 mg per serving

GABA is a calming chemical messenger (neurotransmitter) that your body makes on its own, and it is sold as a supplement for stress, anxiety, and sleep...

GABA monograph & interactions

DMAE (Dimethylaminoethanol) Bitartrate

Interacts with
219 drugs
125 mg per serving

Deanol (DMAE) is a compound related to choline that is marketed for memory, focus, and mood, but solid human evidence for most of these uses is limite...

DMAE (Dimethylaminoethanol) Bitartrate monograph & interactions

Soy Lecithin

No known
interactions
200 mg per serving Form: Alpha-Glycerylphosphorylcholine, Total Phosphatidylcholine

Lecithin is a natural fatty substance found in foods and made by the body that is widely used as a supplement and food emulsifier. Evidence supporting...

Soy Lecithin monograph & interactions

Omega-3 Complex

Interacts with
375 drugs
15 mg per serving Form: high refined Fish Oil, Total EPA & DHA

DHA is an omega-3 fatty acid found in fatty fish and algae that is a building block for the brain, nervous system, and eyes. It is widely used and gen...

Omega-3 Complex monograph & interactions

Ginkgo biloba extract

Interacts with
1,266 drugs
60 mg per serving Form: Flavone Glycosides, Terpene Lactones

Ginkgo is one of the world's most popular herbal supplements, mostly taken to support memory and circulation. The evidence for these uses is mixed and...

Ginkgo biloba extract monograph & interactions

Caffeine

Interacts with
655 drugs
50 mg per serving Form: Green Tea

Caffeine is a natural stimulant found in coffee, tea, and many other plants and products. In moderate amounts it can boost alertness and reduce tiredn...

Caffeine monograph & interactions

Huperzia serrata extract

Interacts with
219 drugs
100 mcg per serving Form: Huperzine-A

Toothed Clubmoss is a moss-like plant best known as the natural source of huperzine A, a compound studied mainly for memory and Alzheimer's disease. S...

Huperzia serrata extract monograph & interactions

Other (inactive) ingredients: Calcium Carbonate, Microcrystalline Cellulose, Stearic Acid, Croscarmellose Sodium, Coating, Crospovidone, Magnesium Stearate, Silica. These complete the product’s ingredient list but are not active constituents.

Interaction report

Focus Formula by Focus Formula Drug Interactions

Focus Formula contains 9 ingredients, and 8 of them have known drug interactions. Altogether they interact with 1,624 medications. Here’s the picture, then you can look up your own drug.

Want to check YOUR meds against Focus Formula?

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
1,624Drugs
9 Major 1,568 Moderate 47 Minor

Ingredients driving the most interactions

Ginkgo biloba extract 1,266
Caffeine 655
GABA 419
Omega-3 Complex 375
Alpha-Lipoic Acid 263

Individual Drug Interactions

The ingredients in Focus Formula interact with 1,624 drugs. Click any drug to see the details.

8 of the 9 ingredients in Focus Formula interact with drugs. Each result below shows which ingredient is responsible. Ginkgo biloba extract Caffeine GABA Omega-3 Complex Alpha-Lipoic Acid DMAE (Dimethylaminoethanol) Bitartrate Huperzia serrata extract Vinpocetine

Each ingredient & the kinds of drugs it affects

For each ingredient in Focus Formula with known interactions, here are the types of medications they can affect. Open any type for the detail — or search your exact drug in the checker above.

Ginkgo biloba extract23 drug types · 1,266 drugs

Talinolol

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

Likelihood Probable Evidence B
Alprazolam (Xanax)

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

Likelihood Probable Evidence B
Anticoagulant/Antiplatelet Drugs

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

Likelihood Possible Evidence A
Anticonvulsants

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

Likelihood Possible Evidence D
Antidiabetes Drugs

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

Likelihood Possible Evidence B
Atorvastatin (Lipitor)

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

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

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

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

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

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

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

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

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

Likelihood Possible Evidence B
Efavirenz (Sustiva)

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

Likelihood Possible Evidence D
Ibuprofen (Advil, Others)

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

Likelihood Possible Evidence D
P-Glycoprotein Substrates

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

Likelihood Possible Evidence B
Risperidone (Risperdal)

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

Likelihood Possible Evidence D
Rosiglitazone (Avandia)

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

Likelihood Possible Evidence D
Seizure Threshold Lowering Drugs

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

Likelihood Possible Evidence D
Simvastatin (Zocor)

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

Likelihood Probable Evidence B
Sofosbuvir (Sovaldi)

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

Likelihood Possible Evidence D
Tacrolimus (Prograf)

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

Likelihood Possible Evidence D
Trazodone (Desyrel)

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

Likelihood Possible Evidence D
Warfarin (Coumadin)

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

Likelihood Possible Evidence B
Nifedipine (Procardia)

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

Likelihood Possible Evidence B
Omeprazole (Prilosec)

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

Likelihood Possible Evidence B
Ginkgo biloba extract full monograph & interactions

Caffeine41 drug types · 655 drugs

Ephedrine

Theoretically, concomitant use might increase the risk for stimulant adverse effects.
Use of ephedrine with caffeine can increase the risk of stimulatory adverse effects. 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 Probable Evidence D
Adenosine (Adenocard)

Theoretically, caffeine might decrease the vasodilatory effects of adenosine and interfere with its use prior to stress testing.
Some evidence shows that caffeine is a competitive inhibitor of adenosine and can reduce the vasodilatory effects of adenosine in humans. However, other research shows that 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 (Persantine) than adenosine-induced stress testing.

Likelihood Possible Evidence B
Anticoagulant/Antiplatelet Drugs

Theoretically, caffeine may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
Caffeine is reported to have antiplatelet activity. Theoretically, it might increase the risk of bleeding when used concomitantly with these agents; however, this interaction has not been reported in humans.

Likelihood Possible Evidence D
Beta-Adrenergic Agonists

Theoretically, large amounts of caffeine might increase the cardiac inotropic effects of beta-agonists.

Likelihood Probable Evidence D
Carbamazepine (Tegretol)

Theoretically, caffeine might reduce the effects of carbamazepine and increase the risk for convulsions.
Animal research suggests that taking caffeine can lower the anticonvulsant effects of carbamazepine and can induce seizures when taken in doses above 400 mg/kg. Human research has shown that taking caffeine 300 mg in three divided doses along with carbamazepine 200 mg reduces the bioavailability of carbamazepine by 32% and prolongs the plasma half-life of carbamazepine 2-fold in healthy individuals.

Likelihood Possible Evidence D
Cimetidine (Tagamet)

Theoretically, cimetidine might increase the levels and adverse effects of caffeine.
Cimetidine decreases the rate of caffeine clearance by 31% to 42%.

Likelihood Likely Evidence B
Clozapine (Clozaril)

Caffeine might increase the levels and adverse effects of clozapine and acutely exacerbate psychotic symptoms.
Caffeine might increase the effects and toxicity of clozapine. Caffeine doses of 400-1000 mg per day inhibit clozapine metabolism. Clozapine is metabolized by cytochrome P450 1A2 (CYP1A2). Although researchers speculate that caffeine might inhibit CYP1A2, there is no reliable evidence that caffeine affects CYP1A2. There is also speculation that genetic factors might make some patients more sensitive to an interaction between clozapine and caffeine. In one case report, severe, life-threatening clozapine toxicity and multiorgan system failure occurred in a patient with schizophrenia stabilized on clozapine who consumed caffeine 600 mg daily.

Likelihood Possible Evidence B
Dipyridamole (Persantine)

Theoretically, caffeine might decrease the vasodilatory effects of dipyridamole and interfere with its use prior to stress testing.
Caffeine inhibits 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 (Persantine) than adenosine-induced stress testing.

Likelihood Probable Evidence B
Disulfiram (Antabuse)

Theoretically, disulfiram use might increase the levels and adverse effects of caffeine.
Disulfiram decreases the rate of caffeine clearance.

Likelihood Probable Evidence B
Diuretic Drugs

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

Likelihood Possible Evidence D
Estrogens

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

Likelihood Probable Evidence B
Ethosuximide (Zarontin)

Theoretically, caffeine might reduce the effects of ethosuximide and increase the risk for convulsions.
Animal research suggests that caffeine 92.4 mg/kg can decrease the anticonvulsant activity of ethosuximide. However, this effect has not been reported in humans.

Likelihood Possible Evidence D
Felbamate (Felbatol)

Theoretically, caffeine might reduce the effects of felbamate and increase the risk for convulsions.
Animal research suggests that a high dose of caffeine 161.7 mg/kg can decreases the anticonvulsant activity of felbamate. However, this effect has not been reported in humans.

Likelihood Possible Evidence D
Flutamide (Eulexin)

Theoretically, caffeine might increase the levels and adverse effects of flutamide.
In vitro evidence suggests that caffeine can inhibit the metabolism of flutamide. However, this effect has not been reported in humans.

Likelihood Probable Evidence D
Fluvoxamine (Luvox)

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

Likelihood Probable Evidence D
Lithium

Abrupt caffeine withdrawal might increase the levels and adverse effects of lithium.
Caffeine has diuretic activity. When abruptly discontinued, caffeine may alter the clearance of lithium. There are two case reports of lithium tremor that worsened upon abrupt coffee withdrawal and 6 case reports of elevated serum lithium levels after reducing or eliminating caffeine intake. In one case, a male with schizoaffective disorder stabilized on lithium had an elevated lithium level after reducing his caffeine intake by 87%. At a later date, he increased his caffeine intake by 6-fold, resulting in a subtherapeutic lithium level and a recurrence of psychiatric symptoms.

Likelihood Probable Evidence D
Monoamine Oxidase Inhibitors (Maois)

Theoretically, concomitant use might increase the risk of a hypertensive crisis.
Caffeine has been shown to inhibit monoamine oxidase (MAO) A and B in laboratory studies. Concomitant intake of large amounts of caffeine with MAOIs might precipitate a hypertensive crisis. In a case report, a patient that consumed 10-12 cups of caffeinated coffee and took the MAOI tranylcypromine presented with severe hypertension. Hypertension was resolved after the patient switched to drinking decaffeinated coffee.

Likelihood Possible Evidence D
Nicotine

Theoretically, concomitant use might increase the risk of hypertension.
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, caffeine might decrease the effects of pentobarbital.
Caffeine might negate the hypnotic effects of pentobarbital.

Likelihood Possible Evidence B
Phenobarbital (Luminal)

Theoretically, caffeine might reduce the effects of phenobarbital and increase the risk for convulsions.
Animal research suggests that caffeine can decrease the anticonvulsant activity of phenobarbital. However, 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.
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, caffeine might reduce the effects of phenytoin and increase the risk for convulsions.
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
Pioglitazone (Actos)

Theoretically, caffeine might increase the levels and clinical effects of pioglitazone.
Animal research suggests that caffeine can modestly increase the maximum concentration, area under the curve, and half-life of pioglitazone, and also reduce its clearance. This increased the antidiabetic effects of pioglitazone. 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.
Quinolones (also called fluoroquinolones) can decrease caffeine clearance by inhibiting cytochrome P450 1A2 (CYP1A2) enzyme.

Likelihood Probable Evidence B
Riluzole (Rilutek)

Theoretically, concomitant use might increase the levels and adverse effects of both caffeine and riluzole.
Caffeine and riluzole are both metabolized by cytochrome P450 1A2 (CYP1A2), and concomitant use might reduce the metabolism of one or both agents.

Likelihood Possible Evidence D
Caffeine full monograph & all 41 interactions

GABA2 drug types · 419 drugs

Antihypertensive Drugs

Theoretically, taking GABA with antihypertensive drugs might increase the risk of hypotension.
Some clinical research shows that GABA can decrease blood pressure in patients with hypertension.

Likelihood Possible Evidence B
Cns Depressants

Theoretically, GABA might have additive sedative effects when used in conjunction with CNS depressants. However, it is unclear if this concern is clinically relevant.
Endogenous GABA has well-established relaxant effects and GABA(A) receptors have an established physiological role in sleep. However, the effects of GABA supplements are unclear, as it is unknown whether exogenous GABA crosses the blood-brain barrier. Although there have been limited reports of drowsiness or tiredness with GABA supplements, these effects have not been widely reported in clinical studies. Additionally, intravenous GABA 0.1-1 mg/kg has been shown to induce anxiety in a dose-dependent manner.

Likelihood Unlikely Evidence D
GABA full monograph & interactions

Omega-3 Complex3 drug types · 375 drugs

Anticoagulant/Antiplatelet Drugs

Theoretically, DHA may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
Although some clinical evidence suggests that DHA might reduce collagen-stimulated platelet aggregation and thromboxane release, most clinical evidence suggests that DHA alone does not affect blood clotting. However, theoretically, when given in combination with EPA as fish oil, concomitant use with anticoagulant or antiplatelet drugs (including aspirin) might increase risk of bleeding.

Likelihood Unlikely Evidence B
Antidiabetes Drugs

Theoretically, taking DHA with antidiabetes drugs might reduce the effects of these medications.
In people with type 2 diabetes, including those taking oral hypoglycemic medications, DHA seems to increase fasting blood glucose levels.

Likelihood Possible Evidence B
Antihypertensive Drugs

Theoretically, taking DHA with antihypertensive drugs might increase the risk of hypotension.
Fish oils containing DHA can lower blood pressure and might have additive effects in patients treated with antihypertensives; use with caution.

Likelihood Probable Evidence B
Omega-3 Complex full monograph & interactions

Alpha-Lipoic Acid5 drug types · 263 drugs

Alkylating Agents

Theoretically, the antioxidant effects of alpha-lipoic acid might alter the effectiveness of alkylating agents.
The use of antioxidants like alpha-lipoic acid during chemotherapy is controversial. There are concerns that antioxidants could reduce the activity of chemotherapy drugs that generate free radicals. However, some researchers theorize that antioxidants might make chemotherapy more effective by reducing oxidative stress that might interfere with apoptosis (cell death) of cancer cells. More evidence is needed to determine what effect, if any, antioxidants such as alpha-lipoic acid have on chemotherapy. Advise patients to consult their oncologist before using alpha-lipoic acid.

Likelihood Possible Evidence D
Anticoagulant/Antiplatelet Drugs

Theoretically, alpha-lipoic acid may have antiplatelet effects and may increase the risk of bleeding if used with anticoagulant or antiplatelet drugs.
In vitro, alpha-lipoic acid inhibits platelet aggregation.

Likelihood Possible Evidence D
Antitumor Antibiotics

Theoretically, the antioxidant effects of alpha-lipoic acid might alter the effectiveness of antitumor antibiotics.
The use of antioxidants like alpha-lipoic acid during chemotherapy is controversial. There are concerns that antioxidants could reduce the activity of antitumor antibiotic drugs, which work by generating free radicals. However, some researchers theorize that antioxidants might make chemotherapy more effective by reducing oxidative stress that might interfere with apoptosis (cell death) of cancer cells. More evidence is needed to determine what effect, if any, antioxidants such as alpha-lipoic acid have on chemotherapy involving antitumor antibiotics. Advise patients to consult their oncologist before using alpha-lipoic acid.

Likelihood Possible Evidence D
Thyroid Hormone

Theoretically, alpha-lipoic acid might decrease the effects of thyroid hormone drugs.
Animal research suggests that co-administration of thyroxine with alpha-lipoic acid reduces conversion into the active T3 form.

Likelihood Possible Evidence D
Antidiabetes Drugs

Theoretically, taking alpha-lipoic acid with antidiabetes drugs might increase the risk of hypoglycemia.
Although some small clinical studies have suggested that alpha-lipoic acid can lower blood glucose levels, larger clinical studies in patients with diabetes have shown no clinically meaningful effect. Additionally, co-administration of single doses of alpha-lipoic acid and glyburide or acarbose did not cause detectable drug interactions in healthy volunteers.

Likelihood Unlikely Evidence B
Alpha-Lipoic Acid full monograph & interactions

DMAE (Dimethylaminoethanol) Bitartrate2 drug types · 219 drugs

Anticholinergic Drugs

Theoretically, deanol might decrease the effectiveness of anticholinergic drugs.
Deanol is thought to increase acetylcholine levels.

Likelihood Unlikely Evidence D
Cholinergic Drugs

Theoretically, deanol might increase the effects and adverse effects of cholinergic drugs.
Deanol is thought to increase acetylcholine levels.

Likelihood Unlikely Evidence D
DMAE (Dimethylaminoethanol) Bitartrate full monograph & interactions

Huperzia serrata extract2 drug types · 219 drugs

Anticholinergic Drugs

In animal models, toothed clubmoss and huperzine A, an active constituent of toothed clubmoss, reversed cognitive deficits induced by scopolamine. Theoretically, concurrent use of anticholinergic drugs and toothed clubmoss might decrease the effectiveness of toothed clubmoss or the anticholinergic drug.
Some anticholinergic drugs include atropine, benztropine (Cogentin), biperiden (Akineton), procyclidine (Kemadrin), and trihexyphenidyl (Artane).

Likelihood Possible Evidence D
Cholinergic Drugs

Huperzine A, a constituent of toothed clubmoss, has demonstrated acetylcholinesterase inhibitory properties. Theoretically, concurrent use of toothed clubmoss with cholinergic drugs might have additive effects and increase the risk of cholinergic side effects.
Cholinergic drugs include bethanechol (Urecholine), donepezil (Aricept), echothiophate (Phospholine Iodide), edrophonium (Enlon, Reversol, Tensilon), neostigmine (Prostigmin), physostigmine (Antilirium), pyridostigmine (Mestinon, Regonol), succinylcholine (Anectine, Quelicin), and tacrine (Cognex).

Likelihood Possible Evidence D
Huperzia serrata extract full monograph & interactions

Vinpocetine3 drug types · 208 drugs

Anticoagulant/Antiplatelet Drugs

Vinpocetine might increase the risk of bleeding when taken with anticoagulant or antiplatelet drugs.
Clinical research shows that vinpocetine decreases red blood cell aggregation, as well as plasma and whole blood viscosity. This effect has been seen with intravenous vinpocetine 1 mg/kg and oral vinpocetine 30 mg daily. Vinpocetine also seems to have antiplatelet effects.

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

Theoretically, vinpocetine might increase levels of drugs metabolized by CYP2C9.
In vitro research shows that vinpocetine weakly inhibits CYP2C9. However, this effect has not been reported in humans.

Likelihood Possible Evidence D
Warfarin (Coumadin)

Vinpocetine might modestly increase the risk of bleeding when taken with warfarin.
Clinical research shows that the combination of warfarin and vinpocetine leads to slight increases in prothrombin time and the area under the concentration curve for warfarin. However, these increases were small, and researchers suggest that this interaction is not likely to be clinically significant in most patients.

Likelihood Possible Evidence B
Vinpocetine full monograph & interactions
The maker

Brand information

Manufacturer and brand details for Focus Formula, from the product label.

Focus Formula

See all Focus Formula products
Name
Windmill Health Products
Street Address
10 Henderson Drive
City
West Caldwell
State
NJ
ZipCode
07006
Pharmacist Counseling Corner

Focus Formula by Focus Formula: Common Questions

Does Focus Formula by Focus Formula interact with any medications?
Yes. Based on its ingredients, Focus Formula has a known interaction with 1,624 medications, including 9 rated major. Use the checker to see how it interacts with a specific drug.
How can one product interact with so many drugs?
Focus Formula contains 9 active ingredients, and an interaction can come from any of them. We check every ingredient, combine the results into one list per medication, and show which ingredient and mechanism is responsible.
Where does this information come from?
The product label data comes from the NIH Dietary Supplement Label Database (DSLD); the interaction data is built on the Natural Medicines database and reviewed by HelloPharmacist pharmacists.

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

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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.

Focus Formula label
Go deeper

The Full Monographs Behind Focus Formula’s Ingredients

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

Herb & supplement monograph

Alpha-lipoic Acid

Interacts with 263 drugs

Alpha-lipoic acid (ALA) is an antioxidant made naturally by the body and found in small amounts in foods. It is most studied for diabetic nerve pain, where some evidence suggests it may help...

Read the full Alpha-lipoic Acid monograph → Herb & supplement monograph

Vinpocetine

Interacts with 208 drugs

Vinpocetine is a lab-made compound based on a chemical from the periwinkle plant, and it is marketed mainly for memory and brain health. The evidence behind these uses is limited and not str...

Read the full Vinpocetine monograph → Herb & supplement monograph

Gamma-aminobutyric Acid (gaba)

Interacts with 419 drugs

GABA is a calming chemical messenger (neurotransmitter) that your body makes on its own, and it is sold as a supplement for stress, anxiety, and sleep. The science behind oral GABA supplemen...

Read the full Gamma-aminobutyric Acid (gaba) monograph → Herb & supplement monograph

Deanol

Interacts with 219 drugs

Deanol (DMAE) is a compound related to choline that is marketed for memory, focus, and mood, but solid human evidence for most of these uses is limited or mixed. It can cause side effects in...

Read the full Deanol monograph → Herb & supplement monograph

Lecithin

Lecithin is a natural fatty substance found in foods and made by the body that is widely used as a supplement and food emulsifier. Evidence supporting most of its health claims is limited, t...

Read the full Lecithin monograph → Herb & supplement monograph

Docosahexaenoic Acid (dha)

Interacts with 375 drugs

DHA is an omega-3 fatty acid found in fatty fish and algae that is a building block for the brain, nervous system, and eyes. It is widely used and generally well tolerated, with the stronges...

Read the full Docosahexaenoic Acid (dha) monograph → Herb & supplement monograph

Ginkgo

Interacts with 1,266 drugs

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

Read the full Ginkgo monograph → Herb & supplement monograph

Caffeine

Interacts with 655 drugs

Caffeine is a natural stimulant found in coffee, tea, and many other plants and products. In moderate amounts it can boost alertness and reduce tiredness for most healthy adults, but too muc...

Read the full Caffeine monograph → Herb & supplement monograph

Toothed Clubmoss

Interacts with 219 drugs

Toothed Clubmoss is a moss-like plant best known as the natural source of huperzine A, a compound studied mainly for memory and Alzheimer's disease. Some early research is promising, but the...

Read the full Toothed Clubmoss monograph →
Sources

Sources & How We Checked

Focus Formula'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 496 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.

Alpha-lipoic Acid 48 references
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  2. Anon. Alpha-lipoic acid. Altern Med Rev 1998;3:308-10.
  3. Konrad T, Vicini P, Kusterer K, et al. Alpha-lipoic acid treatment decreases serum lactate and pyruvate concentrations and improves glucose effectiveness in lean and obese patients with Type 2 diabetes. Diabetes Care 1999;22:280-7. PubMed
  4. Ziegler D, Hanefeld M, Ruhnau KJ, et al. Treatment of symptomatic diabetic peripheral neuropathy with the antioxidant alpha-lipoic acid: A 3-week, multicentre randomized controlled trial (ALADIN Study). Diabetologia 1995;38:1425-33.
  5. Gleiter CH, Schreeb KH, Freudenthaler S, et al. Lack of interaction between thioctic acid, glibenclamide and acarbose. Br J Clin Pharmacol 1999;48:819-25. PubMed
  6. Jacob S, Henriksen EJ, Tritschler HJ, et al. Improvement of insulin-stimulated glucose-disposal in type 2 diabetes after repeated parenteral administration of thioctic acid. Exp Clin Endocrinol Diabet 1996;104:284-8. PubMed
  7. Jacob S, Henriksen EJ, Schiemann AL, et al. Enhancement of glucose disposal in patients with type 2 diabetes by alpha-lipoic acid. Arzneimittelforschung 1995;45:872-4.
  8. Jacob S, Ruus P, Hermann R, et al. Oral administration of RAC-alpha-lipoic acid modulates insulin sensitivity in patients with type-2 diabetes mellitus: a placebo-controlled, pilot trial. Free Rad Biol Med 1999;27:309-14.
  9. Segermann J, Hotze A, Ulrich H, Rao GS. Effect of alpha-lipoic acid on the peripheral conversion of thyroxine to triiodothyronine and on serum lipid-, protein- and glucose levels. Arzneimittelforschung 1991;41:1294-8.
  10. Beitner H. Randomized, placebo controlled, double-blind study on the clinical efficacy of a cream containing 5% alpha-lipoic acid related to photoaging of facial skin. Br J Dermatol 2003;149:841-9.
  11. Ziegler D, Nowak H, Kempler P, et al. Treatment of symptomatic diabetic polyneuropathy with the antioxidant alpha-lipoic acid: A meta-analysis. Diabet Med 2004;21:114-21.
  12. Prasad KN. Rationale for using high-dose multiple dietary antioxidants as an adjunct to radiation therapy and chemotherapy. J Nutr 2004;134:3182S-3S. PubMed
  13. Conklin KA. Cancer chemotherapy and antioxidants. J Nutr 2004;134:3201S-3204S. PubMed
  14. Vincent HK, Bourguignon CM, Vincent KR, Taylor AG. Effects of alpha-lipoic acid supplementation in peripheral arterial disease: a pilot study. J Alt Complement Med 2007;13:577-84. PubMed
  15. Furukawa N, Miyamura N, Nishida K, et al. Possible relevance of alpha lipoic acid contained in a health supplement in a case of insulin autoimmune syndrome. Diabetes Res Clin Pract 2007;75:366-7. PubMed
  16. Ziegler D., Ametov A., Barinov A., Dyck P. J., Gurieva I., Low P. A., Munzel U., Yakhno N., Raz I., Novosadova M., Maus J., Samigullin, R. Oral treatment with alpha-lipoic acid improves symptomatic diabetic polyneuropathy: the SYDNEY 2 trial. Diabetes Car
  17. Gu X. M., Zhang S. S., Wu J. C., Tang Z. Y., Lu Z. Q., Li H., Liu C., Chen L., Ning, G. [Efficacy and safety of high-dose a-lipoic acid in the treatment of diabetic polyneuropathy]. Zhonghua Yi Xue Za Zhi 2010;90(35):2473-2476.
  18. Porasuphatana S., Suddee S., Nartnampong A., Konsil J., Harnwong B., Santaweesuk A. Glycemic and oxidative status of patients with type 2 diabetes mellitus following oral administration of alpha-lipoic acid: a randomized double-blinded placebo-controlled
  19. Ansar H., Mazloom Z., Kazemi F., Hejazi N. Effect of alpha-lipoic acid on blood glucose, insulin resistance and glutathione peroxidase of type 2 diabetic patients. Saudi Med J 2011;32(6):584-588. DOI
  20. de Oliveira A. M., Rondó P. H., Luzia L. A., D'Abronzo F. H., Illison V. K. The effects of lipoic acid and a-tocopherol supplementation on the lipid profile and insulin sensitivity of patients with type 2 diabetes mellitus: a randomized, double-blind, pla
  21. Mazloom Z., Ansar H. The Effect of Alpha-Lipoic Acid on Blood Pressure in Type 2 Diabetics. Iranian Journal of Endocrinology and Metabolism 2009;11(3):245-250.
  22. Volchegorskii I. A., Rassokhina L. M., Koliadich M. I., Alekseev M. I. [Comparative study of alpha-lipoic acid and mexidol effects on affective status, cognitive functions and quality of life in diabetes mellitus patients]. Eksp Klin Farmakol 2011;74(11):
  23. Cavalcanti D. R., da Silveira F. R. Alpha lipoic acid in burning mouth syndrome--a randomized double-blind placebo-controlled trial. J Oral Pathol Med 2009;38(3):254-261. PubMed
  24. Koh E. H., Lee W. J., Lee S. A., Kim E. H., Cho E. H., Jeong E., Kim D. W., Kim M. S., Park J. Y., Park K. G., Lee H. J., Lee I. K., Lim S., Jang H. C., Lee K. H., Lee K. U. Effects of alpha-lipoic Acid on body weight in obese subjects. Am J Med 2011;124( PubMed
  25. Bergqvist-Karlsson, A., Thelin, I., and Bergendorff, O. Contact dermatitis to alpha-lipoic acid in an anti-wrinkle cream. Contact Dermatitis 2006;55(1):56-57.
  26. Tang, J., Wingerchuk, D. M., Crum, B. A., Rubin, D. I., and Demaerschalk, B. M. Alpha-lipoic acid may improve symptomatic diabetic polyneuropathy. Neurologist. 2007;13(3):164-167. PubMed
  27. Hegazy SK, Tolba OA, Mostafa TM, Eid MA, El-Afify DR. Alpha-lipoic acid improves subclinical left ventricular dysfunction in asymptomatic patients with type 1 diabetes. Rev Diabet Stud 2013;10(1):58-67. PubMed
  28. Huang Z, Wan X, Liu J, et al. Short-term continuous subcutaneous insulin infusion combined with insulin sensitizers rosiglitazone, metformin, or antioxidant a-lipoic acid in patients with newly diagnosed type 2 diabetes mellitus. Diabetes Technol Ther 201
  29. Sarezky D, Raquib AR, Dunaief JL, Kim BJ. Tolerability in the elderly population of high-dose alpha lipoic acid: a potential antioxidant therapy for the eye. Clin Ophthalmol. 2016 Sep 29;10:1899-1903. PubMed
  30. Boriani F, Granchi D, Roatti G, Merlini L, Sabattini T, Baldini N. Alpha-lipoic acid after median nerve decompression at the carpal tunnel: a randomized controlled trial. J Hand Surg Am. 2017 Apr;42(4):236-42. PubMed
  31. Karkabounas S, Papadopoulos N, Anastasiadou C, et al. Effects of a-lipoic Acid, carnosine, and thiamine supplementation in obese patients with type 2 diabetes mellitus: A randomized, double-blind study. J Med Food. 2018;21(12):1197-1203.
  32. Murray GL, Colombo J. (r)Alpha lipoic acid is a safe, effective pharmacologic therapy of chronic orthostatic hypotension associated with low sympathetic tone. Int J Angiol. 2019;28(3):188-193. PubMed
  33. Bobe G, Michels AJ, Zhang WJ, et al. A randomized controlled trial of long-term (R)-&alpha;-lipoic acid supplementation promotes weight loss in overweight or obese adults without altering baseline elevated plasma triglyceride concentrations. J Nutr. 2020:
  34. Passiatore M, Perna A, De-Vitis R, Taccardo G. The use of alfa-lipoic acid-R (ALA-R) in patients with mild-moderate carpal tunnel syndrome: A randomised controlled open label prospective study. Malays Orthop J. 2020;14(1):1-6. PubMed
  35. El-Nahas MR, Elkannishy G, Abdelhafez H, Elkhamisy ET, El-Sehrawy AA. Oral alpha lipoic acid treatment for symptomatic diabetic peripheral neuropathy: A randomized double-blinded placebo-controlled study. Endocr Metab Immune Disord Drug Targets. 2020. PubMed
  36. Kim BJ, Hunter A, Brucker AJ, et al. Orally administered alpha lipoic acid as a treatment for geographic atrophy: A randomized clinical trial. Ophthalmol Retina. 2020;4(9):889-898. PubMed
  37. Derosa G, D'Angelo A, Preti P, Maffioli P. Safety and efficacy of alpha lipoic acid during 4 years of observation: A retrospective, clinical trial in healthy subjects in primary prevention. Drug Des Devel Ther. 2020;14:5367-5374.
  38. Sun Y, Guan X, Wang H, et al. Randomized clinical trial of combined therapy with oral a-lipoic acid and NB-UVB for nonsegmental stable vitiligo. Dermatol Ther. 2021;34(1):e14610.
  39. Gilron I, Robb S, Tu D, et al. Double-blind, randomized, placebo-controlled crossover trial of alpha-lipoic acid for the treatment of fibromyalgia pain: the IMPALA trial. Pain. 2021;162(2):561-568. PubMed
  40. Gullo D, Evans JL, Sortino G, Goldfine ID, Vigneri R. Insulin autoimmune syndrome (Hirata Disease) in European Caucasians taking a-lipoic acid. Clin Endocrinol (Oxf). 2014;81(2):204-9.
  41. Yukina M, Nuralieva N, Solovyev M, Troshina E, Vasilyev E. Insulin autoimmune syndrome. Endocrinol Diabetes Metab Case Rep. 2020;2020:19-0159. PubMed
  42. Moffa S, Improta I, Rocchetti S, Mezza T, Giaccari A. Potential cause-effect relationship between insulin autoimmune syndrome and alpha lipoic acid: Two case reports. Nutrition. 2019;57:1-4. PubMed
  43. Izzo V, Greco C, Corradini D, et al. Insulin autoimmune syndrome in an Argentine woman taking a-lipoic acid: A case report and review of the literature. SAGE Open Med Case Rep. 2018;6:2050313X18819601.
  44. EFSA Panel on Nutrition, Novel Foods and Food Allergens (NDA), Turck D, et al. Scientific opinion on the relationship between intake of alpha-lipoic acid (thioctic acid) and the risk of insulin autoimmune syndrome. EFSA J 2021;19(6):e06577. PubMed
  45. Jibril AT, Jayedi A, Shab-Bidar S. Efficacy and safety of oral alpha-lipoic acid supplementation for type 2 diabetes management: a systematic review and dose-response meta-analysis of randomized trials. Endocr Connect 2022;11(10):e220322. PubMed
  46. Corazza M, Arlotti E, Schettini N, Pacetti L, Bianchi A, Borghi A. Allergic contact dermatitis due to a-lipoic acid in a topical over-the-counter product: A case report. Contact Dermatitis 2023.
  47. Velasco-Amador JP, Prados-Carmona Á, Navarro-Triviño FJ. Contact urticaria syndrome caused by alpha-lipoic acid in a master formula for vulvar lichen sclerosus. Contact Dermatitis 2023;89(2):136-137. PubMed
  48. Sehgal T, Ohri U, Mittal N, Attri P, Dishant F. A Case of Insulin Autoimmune Syndrome in an Indian Male Taking Alpha-Lipoic Acid. Cureus 2023;15(8):e43743. PubMed

See these in context on the Alpha-lipoic Acid monograph →

Vinpocetine 27 references
  1. Hindmarch I, Fuchs HH, Erzigkeit H. Efficacy and tolerance of vinpocetine in ambulant patients suffering from mild to moderate organic psychosyndromes. Int Clin Psychopharmacol 1991;6:31-43. PubMed
  2. Balestreri R, Fontana L, Astengo F. A double-blind placebo controlled evaluation of the safety and efficacy of vinpocetine in the treatment of patients with chronic vascular senile cerebral dysfunction. J Am Geriatr Soc 1987;35:425-30. PubMed
  3. Akopov SE, Gabrielian ES. Effects of aspirin, dipyridamole, nifedipine and cavinton which act on platelet aggregation induced by different aggregating agents alone and in combination. Eur J Clin Pharmacol 1992;42:257-9. PubMed
  4. Kidd PM. A review of nutrients and botanicals in the integrative management of cognitive dysfunction. Altern Med Rev 1999;4:144-61..
  5. Wollschlaeger B. Efficacy of vinpocetine in the management of cognitive impairment and memory loss. JANA 2001;4:25-30.
  6. Hitzenberger G, Sommer W, Grandt R. Influence of vinpocetine on warfarin-induced inhibition of coagulation. Int J Clin Pharmacol Ther Toxicol 1990;28:323-8..
  7. Dekoninck, W. J., Jocquet, P., Jacquy, J., and Henriet, M. Comparative study of the clinical effects of vincamine + glycerol versus glycerol + placebo in the acute phase of stroke. Arzneimittelforschung. 1978;28(9):1654-1657.
  8. Fischhof, P. K., Moslinger-Gehmayr, R., Herrmann, W. M., Friedmann, A., and Russmann, D. L. Therapeutic efficacy of vincamine in dementia. Neuropsychobiology 1996;34(1):29-35. PubMed
  9. Feher, G., Koltai, K., Kesmarky, G., Horvath, B., Toth, K., Komoly, S., and Szapary, L. Effect of parenteral or oral vinpocetine on the hemorheological parameters of patients with chronic cerebrovascular diseases. Phytomedicine. 2009;16(2-3):111-117. PubMed
  10. Kuzuya, F. Effects of vinpocetine on platelet aggregability and erythrocyte deformability. Ther Hung. 1985;33(1):22-34.
  11. Kovacs, L. Cavinton in the treatment of acute stroke. Ther Hung. 1985;33(1):50-57.
  12. Osawa, M. and Maruyama, S. Effects of TCV-3B (vinpocetine) on blood viscosity in ischemic cerebrovascular diseases. Ther.Hung. 1985;33(1):7-12.
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Docosahexaenoic Acid (dha) 49 references
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See these in context on the Ginkgo monograph →

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See these in context on the Toothed Clubmoss monograph →

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

© 2021 Therapeutic Research Center, LLC

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