Amphetalean Ingredients & Drug Interactions
by Beast
What is this page for?
First and foremost: checking Amphetalean 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
Amphetalean is a dietary supplement by Beast with 12 active ingredients. Its ingredients are commonly taken for high cholesterol, vitamin b3 deficiency (pellagra), heart health support.Based on those ingredients, 1,667 medications have a known interaction with it, the most serious rated major. The ingredients most likely to interact are Ginkgo biloba extract, Evodia Rutaecarpa Extract, Higenamine HCl. Use the checker below to test your specific medication, or read the full HelloPharmacist Interaction Report.
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HelloPharmacist Scorecard of Amphetalean by Beast
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
Beast Amphetalean contains 12 active and supporting ingredients. The main actives include niacin (a B vitamin), N,N-dimethyl-tyramine (hordenine, a stimulant), choline bitartrate (a nutrient), cAMP (adenosine), higenamine HCl (a stimulant alkaloid), ginkgo biloba extract (a herbal extract), calcium, phenylethylamine HCl (a stimulant), coffea robusta (coffee extract), raspberry ketones (a phenolic compound), evodia rutaecarpa extract (a herbal extract), and vitamin B1.
The product also contains inactive ingredients including citric acid, glucose polymers, natural and artificial flavors, sucralose, beta-carotene, and acesulfame potassium.
Does it work?
Not established
The evidence for most ingredients in this product is limited or mixed. Niacin is likely effective for pellagra and possibly effective for HIV/AIDS-related dyslipidemia and metabolic syndrome.
Choline shows insufficient evidence for athletic performance, cognitive decline, and several other claims. Ginkgo biloba has possibly effective evidence for hearing loss, stroke recovery, anxiety, dementia, schizophrenia, and premenstrual syndrome.
Calcium is effective for kidney failure and dyspepsia, and likely effective for osteoporosis. The remaining ingredients—hordenine, higenamine, raspberry ketone, and evodia—all carry insufficient or no reliable evidence of effectiveness for their claimed uses in this product.
How safe is it?
Well-documented data
Niacin is generally well tolerated in food amounts but can cause flushing, gastrointestinal upset, and liver problems at high supplement doses—roughly 70% of users experience flushing. High-dose niacin should be avoided in pregnancy unless prescribed.
Hordenine and higenamine have very limited human safety data; hordenine acts as a stimulant and may cause tachycardia and hypertension, while higenamine is banned in competitive sports due to cardiac effects and has rare reports of rhabdomyolysis. Choline is likely safe in pregnancy and generally well tolerated but can cause fishy body odor and gastrointestinal effects at very high doses (above 3.5 grams daily).
Ginkgo is generally well tolerated but carries a known risk of bleeding, especially with other blood thinners, and rare cases of cardiac arrhythmia have been reported—it should be avoided in pregnancy due to bleeding risk. Calcium is generally safe at recommended amounts.
CaMP (adenosine) has safety data primarily from prescription intravenous forms; oral supplement evidence is limited, and it should be avoided during pregnancy and breastfeeding. Evodia has limited human safety data and animal studies show QT prolongation risk; it is traditionally avoided in pregnancy.
Raspberry ketone resembles a stimulant and has rare case reports of serious arrhythmias, though human safety data is very limited.
Meds to double-check
Major interaction found
Before taking Beast Amphetalean, check with your pharmacist or doctor if you take any of the following: HIV integrase inhibitors (dolutegravir, elvitegravir, raltegravir), because calcium in this product can significantly lower their blood levels; blood thinners or antiplatelet drugs (warfarin, aspirin, others), because ginkgo, higenamine, and evodia may increase bleeding risk; blood-pressure medications, because niacin and hordenine may increase hypotension risk or interact with stimulant properties; diabetes medications, because niacin can raise blood sugar; statins or other cholesterol drugs; beta-blockers, because ginkgo may reduce their effectiveness; or gout medications, because niacin may interfere. Additionally, if you take dipyridamole (Persantine), a cardiac stress test drug, the cAMP in this product carries a Major interaction.
Do not combine this product with other stimulants or MAOIs (monoamine oxidase inhibitor antidepressants).
The bottom line
Scorecard at a glanceFormula with limited ingredient disclosure with no established evidence rating for its marketed use. Major medication interactions have been identified, and safety information is well characterized.
This is a multi-ingredient stimulant and thermogenic product with significant medication interactions—especially if you take HIV drugs, blood thinners, heart medications, blood-pressure drugs, or diabetes medications. Talk with your pharmacist or doctor before starting, and check your exact medications using the tool on this page.
The ingredients are generally well tolerated at typical doses, but several (hordenine, higenamine, evodia) have limited human safety data and potent cardiovascular effects.
Educational only — not medical advice; always confirm with your pharmacist. Our editorial policy · How we use AI
Assessment coverage: 9 of 12 active ingredients matched to our full ingredient reviews (monographs). Based on the product label dated Feb 26, 2014.
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 Amphetalean, straight from the product label.
| Brand | Beast |
|---|---|
| Barcode (UPC) | 631312706542 |
| Net contents | 7.93 Oz(s); 225 Gram(s) |
| Market status | On market |
| Date entered into DSLD | Feb 26, 2014 |
| DSLD ID | 30700 |
| Product type | Other Combinations |
| Supplement form | Powder |
| Dietary claims / uses | All Other, Structure/Function |
| Intended target group(s) | Adult (18 - 50 Years) |
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 Amphetalean by Beast, sourced from the NIH Dietary Supplement Label Database.
Supplement Facts
| Ingredient | Amount | % DV |
|---|---|---|
| Calories | 0 Not Present | -- |
| Total Carbohydrates | 0 Not Present | -- |
| Niacin | 10 mg | 50% |
| N,N-Dimethyl-Tyramine | 0 NP | -- |
| Choline Bitartrate | 0 NP | -- |
| cAMP | 0 NP | -- |
| Vitamin B1 | 60 mg | 4000% |
| Higenamine HCl | 0 NP | -- |
| Ginkgo biloba extract | 0 NP | -- |
| Calcium | 63 mg | 6% |
| Amphetalean Thermogenic Matrix | 958 mg | -- |
| Phenylethylamine HCl | 0 NP | -- |
| Coffea robusta | 0 NP | -- |
| Raspberry Ketones | 0 NP | -- |
| Evodia Rutaecarpa Extract | 0 NP | -- |
Other ingredients: Citric Acid, Glucose Polymers, Natural & Artificial flavors, Sucralose, Beta-Carotene, Acesulfame Potassium
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.
General Statements
ALL BEAST PRODUCTS ARE RIGOROUSLY TESTED FOR: ASSAY SHOWING PURITY. MICROBIALS TO DETECT BACTERIA & MOLD. HEAVY METALS INCLUDING MERCURY AND LEAD.
THERMOGENIC ENERGY HELPS BURN BODY FAT AND INCREASES ENERGY LEVELS WHILE ENHANCING MOOD, MENTAL FOCUS, AND CLARITY.
USA_Ver_2.3_DS130322
Brand IP Statement(s)
(TM)B
BEAST(TM) THE STRONGEST NAME IN SPORTS NUTRITION(TM)
GET LEAN. STAY LEAN.(TM)
THE STORY BEHIND AMPHETALEAN(R) Designed for three different purposes, Amphetalean(R) is an energy formula that boosts energy levels and keeps them constant. Some rely on Ampetalean(R) as their pre-workout booster, others use it to burn fat and promote weight loss, while a third group takes Amphetalean(R) during the day to increase mental acuity.
Seals/Symbols
ORANGE COOLER FLAVOR BURN FAT MAXIMIZE FOCUS INCREASE ENERGY
Formula
45 SERVINGS
Contains caffeine.
FDA Statement of Identity
DIETARY SUPPLEMENT
Precautions
ALLERGEN WARNING: This product was produced in a facility that may also process ingredients containing milk, eggs, soybeans, shellfish, fish, tree nuts, and peanuts.
WARNING: CHECK WITH A QUALIFIED HEALTHCARE professional before using this product, or any dietary supplement, if you are under the age of 18 or if you have any known or suspected medical condition(s) and/or are taking any prescription or OTC medication(s).
WARNING: CHECK WITH A QUALIFIED HEALTHCARE professional before using this product, or any dietary supplement, if you are under the age of 18 or if you have any known or suspected medical condition(s) and/or are taking any prescription or OTC medication(s).
Discontinue use and consult your health care professional if you experience any adverse reaction to this product.
Too much caffeine may cause irritability, sleeplessness and occasional rapid heartbeat. To avoid sleeplessness, do not consume within 4 hours of bedtime. Always try to consume at least 64 oz of water daily while using this product. Do not exceed recommended dosage. Do not use if seal is broken or missing.
KEEP OUT OF REACH OF CHILDREN.
Storage
STORAGE CONDITIONS: Store in a cool dry place.
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.
Suggested/Recommended/Usage/Directions
SUGGESTED USE: As a dietary supplement, take 1 scoop twice daily for the first 3 days, then continue with 1 to 2 scoops twice daily. Adjust dose accordingly. Use 8 oz of water per scoop. Do not exceed recommended dosage.
Is this label outdated? Report a formula or label change and our pharmacy team will review it.
Amphetalean by Beast 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 Amphetalean by Beast
These are the 12 active ingredients this product is made of. Select any to open its full monograph.
Serving size5 Gram(s) Dosage formPowder Servings per container45 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.
Niacin
Interacts with727 drugs
Niacin (vitamin B3) is an essential nutrient your body needs for energy and metabolism, and deficiency is uncommon in most developed countries. Prescr...
Niacin monograph & interactionsVitamin B1
Calcium
Interacts with168 drugs
Calcium is an essential mineral your body needs for strong bones, nerve signaling, and muscle function, and supplements can help fill gaps when diet f...
Calcium monograph & interactionsAmphetalean Thermogenic Matrix
- › N,N-Dimethyl-Tyramine
- › Choline Bitartrate
- › CAMP
- › Higenamine HCl
- › Ginkgo biloba extract
- › Phenylethylamine HCl
- › Coffea robusta
- › Raspberry Ketones
- › Evodia Rutaecarpa Extract
Other (inactive) ingredients: Citric Acid, Glucose Polymers, Natural & Artificial flavors, Sucralose, Beta-Carotene, Acesulfame Potassium. These complete the product’s ingredient list but are not active constituents.
Amphetalean by Beast Drug Interactions
HelloPharmacist Interaction Report
Beast Amphetalean is a 12-ingredient powder that carries documented interactions with a substantial number of medications.
The most serious interaction involves calcium, which significantly reduces blood levels of dolutegravir (an HIV integrase inhibitor) by up to 40%—a Major-severity effect requiring a 2- or 6-hour separation between doses.
Read the full breakdown — every affected drug type, severity by severity
Several other Major interactions are documented. Ginkgo biloba extract in this product interacts with talinolol (a beta-blocker), and cAMP interacts with dipyridamole (a blood thinner used for heart conditions), both potentially dangerous combinations.
Calcium also has Major interactions with elvitegravir and ceftriaxone.
Moderate-severity interactions span multiple drug categories: niacin affects blood-pressure medications (risk of dangerously low blood pressure), blood thinners, diabetes drugs, cholesterol-lowering statins, gout medications, and bile acid sequestrants. Hordenine (N,N-dimethyl-tyramine) and higenamine are stimulants that interact with other stimulant drugs and carry cardiovascular risks.
Higenamine also interacts with blood thinners and certain enzyme-metabolized drugs. Ginkgo additionally interacts with warfarin (bleeding risk), several psychiatric and anti-HIV medications, and more.
Evodia rutaecarpa extract affects multiple enzyme-metabolized drugs and has documented QT-prolonging properties.
Additionally, choline bitartrate carries only a Minor interaction with atropine. We could not check three ingredients: Vitamin B1, Phenylethylamine HCl, and Coffea robusta.
Altogether, these interactions span 1,646 individual medications. Please use the medication checker below to verify your exact prescriptions before starting.
Check your own medications below · Editorial policy · How we use AI
Want to check YOUR meds against Amphetalean?
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 Amphetalean interact with 1,667 drugs. Click any drug to see the details.
9 of the 12 ingredients in Amphetalean interact with drugs. Each result below shows which ingredient is responsible. Ginkgo biloba extract Evodia Rutaecarpa Extract Higenamine HCl Niacin N,N-Dimethyl-Tyramine Raspberry Ketones Calcium cAMP Choline Bitartrate
AminophyllineAminophylline
How Aminophylline interacts with Amphetalean — through 1 ingredient. Tap an ingredient for the detail:
CampMethylxanthines Minor
Interaction Summary
Methylxanthines are competitive antagonists of adenosine and can block its pharmacologic effects.
Read the full Camp + Aminophylline interactionAtropineSal-Tropine
How Atropine interacts with Amphetalean — through 1 ingredient. Tap an ingredient for the detail:
Choline BitartrateAtropine Minor
Interaction Summary
Theoretically, choline might decrease the effects of atropine in the brain.
Read the full Choline Bitartrate + Atropine interactionAtropine SulfateAtropine Sulfate, Isopto Atropine
How Atropine Sulfate interacts with Amphetalean — through 1 ingredient. Tap an ingredient for the detail:
Choline BitartrateAtropine Minor
Interaction Summary
Theoretically, choline might decrease the effects of atropine in the brain.
Read the full Choline Bitartrate + Atropine Sulfate interactionAtropine, Benzoic Acid, Hyoscyamine, Methenamine, Methylene Blue, PhenylAtrosept
How Atropine, Benzoic Acid, Hyoscyamine, Methenamine, Methylene Blue, Phenyl interacts with Amphetalean — through 1 ingredient. Tap an ingredient for the detail:
Choline BitartrateAtropine Minor
Interaction Summary
Theoretically, choline might decrease the effects of atropine in the brain.
Read the full Choline Bitartrate + Atropine, Benzoic Acid, Hyoscyamine, Methenamine, Methylene Blue, Phenyl interactionAtropine, Benzoic Acid, Hyoscyamine, Methenamine, Methylene Blue, Phenyl SalicylateUrinary Antiseptic 2, Urised
How Atropine, Benzoic Acid, Hyoscyamine, Methenamine, Methylene Blue, Phenyl Salicylate interacts with Amphetalean — through 1 ingredient. Tap an ingredient for the detail:
Choline BitartrateAtropine Minor
Interaction Summary
Theoretically, choline might decrease the effects of atropine in the brain.
Read the full Choline Bitartrate + Atropine, Benzoic Acid, Hyoscyamine, Methenamine, Methylene Blue, Phenyl Salicylate interactionAtropine, DifenoxinMotofen
How Atropine, Difenoxin interacts with Amphetalean — through 1 ingredient. Tap an ingredient for the detail:
Choline BitartrateAtropine Minor
Interaction Summary
Theoretically, choline might decrease the effects of atropine in the brain.
Read the full Choline Bitartrate + Atropine, Difenoxin interactionAtropine, DiphenoxylateLofene, Lomotil
How Atropine, Diphenoxylate interacts with Amphetalean — through 1 ingredient. Tap an ingredient for the detail:
Choline BitartrateAtropine Minor
Interaction Summary
Theoretically, choline might decrease the effects of atropine in the brain.
Read the full Choline Bitartrate + Atropine, Diphenoxylate interactionAtropine, Hyoscyamine, ScopolamineColytrol
How Atropine, Hyoscyamine, Scopolamine interacts with Amphetalean — through 1 ingredient. Tap an ingredient for the detail:
Choline BitartrateAtropine Minor
Interaction Summary
Theoretically, choline might decrease the effects of atropine in the brain.
Read the full Choline Bitartrate + Atropine, Hyoscyamine, Scopolamine interactionDyphyllineDilor, Dilor-400, Dyflex, Lufyllin, Lufyllin-400, Neothylline
How Dyphylline interacts with Amphetalean — through 1 ingredient. Tap an ingredient for the detail:
CampMethylxanthines Minor
Interaction Summary
Methylxanthines are competitive antagonists of adenosine and can block its pharmacologic effects.
Read the full Camp + Dyphylline interactionDyphylline, GuaifenesinDifil G, Dilex-G, Dilor-G, Dyflex G, Dyline GG, Dyphylline GG +3 more
How Dyphylline, Guaifenesin interacts with Amphetalean — through 1 ingredient. Tap an ingredient for the detail:
CampMethylxanthines Minor
Interaction Summary
Methylxanthines are competitive antagonists of adenosine and can block its pharmacologic effects.
Read the full Camp + Dyphylline, Guaifenesin interactionEdrophonium, AtropineEnlon-Plus
How Edrophonium, Atropine interacts with Amphetalean — through 1 ingredient. Tap an ingredient for the detail:
Choline BitartrateAtropine Minor
Interaction Summary
Theoretically, choline might decrease the effects of atropine in the brain.
Read the full Choline Bitartrate + Edrophonium, Atropine interactionGuaifenesin, OxtriphyllineBrondecon
How Guaifenesin, Oxtriphylline interacts with Amphetalean — through 1 ingredient. Tap an ingredient for the detail:
CampMethylxanthines Minor
Interaction Summary
Methylxanthines are competitive antagonists of adenosine and can block its pharmacologic effects.
Read the full Camp + Guaifenesin, Oxtriphylline interactionOxtriphyllineCholedyl, Choledyl SA
How Oxtriphylline interacts with Amphetalean — through 1 ingredient. Tap an ingredient for the detail:
CampMethylxanthines Minor
Interaction Summary
Methylxanthines are competitive antagonists of adenosine and can block its pharmacologic effects.
Read the full Camp + Oxtriphylline interactionTheobromineTheobromine
How Theobromine interacts with Amphetalean — through 1 ingredient. Tap an ingredient for the detail:
CampMethylxanthines Minor
Interaction Summary
Methylxanthines are competitive antagonists of adenosine and can block its pharmacologic effects.
Read the full Camp + Theobromine interactionEach ingredient & the kinds of drugs it affects
For each ingredient in Amphetalean 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 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%.
Evodia Rutaecarpa Extract
Anticoagulant/Antiplatelet Drugs
Theoretically, taking evodia with antiplatelet or anticoagulant drugs might increase the risk of bruising and bleeding.
In vitro and animal studies show that rutaecarpine, a constituent of evodia, inhibits platelet aggregation.
Caffeine
Theoretically, evodia might decrease the levels and clinical effects of caffeine.
In animal models, evodia extract decreases caffeine levels by up to 71%. Evodia extract induces hepatic cytochrome P450 1A2 (CYP1A2) enzyme, of which caffeine is a substrate.
Chlorzoxazone (Parafon Forte, Paraflex)
Theoretically, evodia might decrease the levels and clinical effects of chlorzoxazone.
Animal research shows that administration of rutaecarpine, a constituent of evodia, with chlorzoxazone reduces the area under the curve (AUC) of chlorzoxazone by 84% and increases its clearance by 646%. This interaction is likely due to induction of cytochrome P450 2E1 (CYP2E1) by rutaecarpine .
Cytochrome P450 1A2 (Cyp1A2) Inhibitors
Theoretically, drugs that inhibit CYP1A2 might increase the levels and clinical effects of evodia.
The evodia constituent rutaecarpine is metabolized by CYP1A2.
Cytochrome P450 1A2 (Cyp1A2) Substrates
Evodia might reduce the levels and clinical effects of CYP1A2 substrates through induction of CYP1A2.
Evodia extract and the evodia constituent rutaecarpine induce hepatic CYP1A2 enzyme activity. Evodia decreases levels of theophylline and caffeine, CYP1A2 substrates, by about 70% in animal models.
Cytochrome P450 2E1 (Cyp2E1) Substrates
Theoretically, evodia might reduce the levels and clinical effects of CYP2E1 substrates through induction of CYP2E1.
Animal research suggests that rutaecarpine, a constituent of evodia, induces CYP2E1 activity. In rats, rutaecarpine increases markers of CYP2E1 activity, and administration of rutaecarpine with chlorzoxazone, a known CYP2E1 substrate, reduces the area under the curve (AUC) of chlorzoxazone by 84% and increases its clearance by 646%.
Cytochrome P450 3A4 (Cyp3A4) Inducers
Theoretically, taking CYP3A4 inducers might decrease the levels and clinical effects of evodia.
Animal research shows that concomitant administration of dexamethasone, a known CYP3A4 inducer, with the alkaloid constituents of evodia significantly reduces the area under the curve (AUC), maximum concentration (Cmax), and half-life of these constituents.
Cytochrome P450 3A4 (Cyp3A4) Inhibitors
Theoretically, CYP3A4 inhibitors might increase the levels and clinical effects of evodia.
Animal research shows that concomitant administration of ketoconazole, a known CYP3A4 inhibitor, with the alkaloid constituents of evodia significantly increases the area under the curve (AUC), maximum concentration (Cmax), and half-life of these constituents.
Cytochrome P450 3A4 (Cyp3A4) Substrates
Theoretically, evodia might increase the levels and clinical effects of CYP3A4 substrates.
In vitro research shows that evodia extract inhibits hepatic CYP3A4. This effect has not been reported in humans.
Qt Interval-Prolonging Drugs
Theoretically, evodia might have an additive effect with drugs that prolong the QT interval, potentially increasing the risk of ventricular arrhythmias.
Evodia has demonstrated dose-dependent activity as a proarrhythmic agent in animal and in vitro studies. Evodia infusion in animals extends the action duration potential and induces prolongation of the QT interval and Torsade de pointes.
Theophylline
Theoretically, evodia might decrease the levels and clinical effects of theophylline.
The evodia constituent rutaecarpine decreases theophylline levels and half-life by about 70% in animal models. This constituent appears to induce hepatic cytochrome P450 1A2 (CYP1A2) enzyme activity, of which theophylline is a substrate. Rutaecarpine is the primary active constituent of evodia; however, it is not known if the whole crude extract of evodia also causes this interaction.
Higenamine HCl
Anticoagulant/Antiplatelet Drugs
Theoretically, higenamine might increase the risk of bleeding or bruising when taken with anticoagulant/antiplatelet drugs.
Animal research shows that higenamine inhibits platelet aggregation and reduces the size of thrombus formation.
Cytochrome P450 2D6 (Cyp2D6) Substrates
Theoretically, higenamine might increase the levels and clinical effects of drugs metabolized by CYP2D6.
In vitro research shows that higenamine inhibits CYP2D6 enzymes. However, this effect has not been reported in humans.
Cytochrome P450 3A4 (Cyp3A4) Substrates
Theoretically, higenamine might increase the levels and clinical effects drugs metabolized by CYP3A4.
In vitro research shows that higenamine inhibits CYP3A4 enzymes by 21%. However, this effect has not been reported in humans.
Stimulant Drugs
Theoretically, higenamine might increase the risk of cardiovascular toxicity when taken with stimulant drugs.
Higenamine has stimulant effects due to agonist activity at beta2-adrenoreceptors. In cardiac muscle, higenamine appears to have a positive inotropic effect and increase heart rate. However, it does not appear to increase blood pressure.
Propranolol (Inderal)
Theoretically, the positive inotropic effects of higenamine might be reduced by propranolol.
Animal research shows that higenamine has a positive inotropic effect on the heart, and administering propranolol appears to block this cardiac effect. In animals, propranolol also appears to inhibit corpus cavernosum relaxation induced by higenamine.
Niacin
Alcohol (Ethanol)
Concomitant use of alcohol and niacin might increase the risk of flushing and hepatotoxicity.
Alcohol can exacerbate the flushing and pruritus associated with niacin. Large doses of niacin might also exacerbate liver dysfunction associated with chronic alcohol use. A case report describes delirium and lactic acidosis in a patient taking niacin 3 grams daily who ingested 1 liter of wine. Advise patients to avoid large amounts of alcohol while taking niacin.
Allopurinol (Zyloprim)
Theoretically, niacin might antagonize the therapeutic effects of uricosurics such as allopurinol.
Large doses of niacin can reduce urinary excretion of uric acid, potentially resulting in hyperuricemia. Doses of uricosurics such as allopurinol might need to be increased to maintain control of gout in patients who start taking niacin. People who have frequent attacks of gout despite uricosuric therapy should avoid niacin.
Anticoagulant/Antiplatelet Drugs
Theoretically, niacin may have additive effects when used with anticoagulant or antiplatelet drugs.
Several cases of clotting factor synthesis deficiency and coagulopathy have been reported in patients taking sustained-release niacin. Also, thrombocytopenia has been reported in patients treated with niacin or niacin plus lovastatin.
Antidiabetes Drugs
Niacin can increase blood glucose levels and may diminish the effects of antidiabetes drugs.
Niacin impairs glucose tolerance in a dose-dependent manner, probably by causing or aggravating insulin resistance and increasing hepatic production of glucose. In diabetes patients, niacin 4.5 grams daily for 5 weeks can increase plasma glucose by an average of 16% and glycated hemoglobin (HbA1c) by 21%. However, lower doses of 1.5 grams daily or less appear to have minimal effects on blood glucose. In some patients, glucose levels increase when niacin is started, but then return to baseline when a stable dose is reached. Up to 35% of patients with diabetes may need adjustments in hypoglycemic therapy when niacin is added.
Antihypertensive Drugs
Theoretically, niacin may increase the risk of hypotension when used with antihypertensive drugs.
The vasodilating effects of niacin can cause hypotension. Furthermore, some clinical evidence suggests that a one-hour infusion of niacin can reduce systolic, diastolic, and mean blood pressure in hypertensive patients. This effect is not observed in normotensive patients.
Bile Acid Sequestrants
Bile acid sequestrants can bind niacin and decrease absorption. Separate administration by 4-6 hours to avoid an interaction.
In vitro studies show that colestipol (Colestid) binds about 98% of available niacin and cholestyramine (Questran) binds 10% to 30%.
Gemfibrozil (Lopid)
Theoretically, concomitant use of niacin and gemfibrozil might increase the risk of myopathy in some patients.
A case of myopathy from concomitant use of niacin and gemfibrozil has been reported. Niacin alone has also been associated with cases of myopathy. Using gemfibrozil with niacin might further increase the risk of developing myopathy.
Hepatotoxic Drugs
Theoretically, concomitant use of niacin and hepatotoxic drugs might increase the risk of hepatotoxicity.
Niacin has been associated with cases of liver toxicity, especially when used in pharmacologic doses. Sustained-release niacin preparations appear to be associated with a higher risk of hepatotoxicity than immediate-release niacin.
Hmg-Coa Reductase Inhibitors ("Statins")
Theoretically, concomitant use of niacin and statins might increase the risk of myopathy and rhabdomyolysis in some patients.
Some case reports have raised concerns that niacin might increase the risk of myopathy and rhabdomyolysis when combined with statins. However, a significantly increased risk of myopathy has not been demonstrated in clinical trials, including those using an FDA-approved combination of lovastatin and niacin (Advicor).
Probenecid (Benemid)
Theoretically, niacin might antagonize the therapeutic effects of uricosurics such as probenecid.
Large doses of niacin reduce urinary excretion of uric acid, potentially causing hyperuricemia. Doses of uricosurics such as probenecid might need to be increased to maintain control of gout in patients who start taking niacin. People who have frequent attacks of gout despite uricosuric therapy should avoid niacin.
Sulfinpyrazone (Anturane)
Theoretically, niacin might antagonize the therapeutic effects of uricosurics such as sulfinpyrazone.
Large doses of niacin reduce urinary excretion of uric acid, potentially causing hyperuricemia. Doses of uricosurics such as sulfinpyrazone might need to be increased to maintain control of gout in patients who start taking niacin. People who have frequent attacks of gout despite uricosuric therapy should avoid niacin.
Thyroid Hormone
Theoretically, niacin might antagonize the therapeutic effects of thyroid hormones.
Clinical research and case reports suggests that taking niacin can reduce serum levels of thyroxine-binding globulin by up to 25% and moderately reduce levels of thyroxine (T4). Patients taking thyroid hormone for hypothyroidism might need dose adjustments when using niacin.
Transdermal Nicotine (Nicoderm)
Theoretically, concomitant use of niacin and transdermal nicotine might increase the risk of flushing and dizziness.
Niacin and nicotine can both cause flushing and dizziness.
Warfarin (Coumadin)
There is limited evidence that niacin may increase the anticoagulant effects of warfarin.
In a case report, a patient on warfarin developed an elevated international normalized ratio (INR) of 3.9 after taking niacin for two weeks. The patient's INR was previously stable, ranging between 2 and 3 in recent months, and no other medication changes were identified. The elevated INR returned to therapeutic range within 4 days following the discontinuation of niacin.
Aspirin
Large doses of aspirin might alter the clearance of niacin.
Aspirin is often used with niacin to reduce niacin-induced flushing. Doses of 80-975 mg aspirin have been used, but 325 mg appears to be optimal. Aspirin also seems to reduce the clearance of niacin by competing for glycine conjugation. Taking aspirin 1 gram seems to reduce niacin clearance by 45%. This is probably a dose-related effect and not clinically significant with the more common aspirin dose of 325 mg.
N,N-Dimethyl-Tyramine
Monoamine Oxidase Inhibitors (Maois)
Hordenine is structurally similar to tyramine In vitro research shows that hordenine is a selective substrate for monoamine oxidase-B in the liver. Theoretically, concomitant use of hordenine with MAOIs might increase blood pressure, potentially leading to a hypertensive crisis.
Some MAOIs include isocarboxazid (Marplan), phenelzine (Nardil), selegiline (Eldepryl, Emsam, Zelapar), and tranylcypromine (Parnate).
Stimulant Drugs
Hordenine is structurally similar to N-methyltyramine and synephrine, constituents in bitter orange known to have stimulant properties. Theoretically, taking hordenine with drugs with stimulant properties might increase the risk of hypertension and other adverse cardiovascular effects.
Some of these drugs include amphetamine, caffeine, methylphenidate, pseudoephedrine, and many others.
Cytochrome P450 2D6 (Cyp2D6) Substrates
Hordenine weakly inhibits cytochrome P450 2D6 (CYP2D6) enzymes in vitro. Theoretically, hordenine might increase the levels of CYP2D6 substrates.
Some of drugs that are CYP2D6 substrates include amitriptyline (Elavil), clozapine (Clozaril), codeine, desipramine (Norpramin), donepezil (Aricept), fentanyl (Duragesic), flecainide (Tambocor), fluoxetine (Prozac), meperidine (Demerol), methadone (Dolophine), metoprolol (Lopressor, Toprol XL), olanzapine (Zyprexa), ondansetron (Zofran), tramadol (Ultram), trazodone (Desyrel), and others.
Raspberry Ketones
Stimulant Drugs
Theoretically, raspberry ketone might increase the risk of adverse cardiovascular effects with stimulant drugs.
Structurally, raspberry ketone resembles synephrine, a known stimulant agent. Heart palpitations, elevated blood pressure, coronary vasospasm, pulseless electrical activity arrest, and resistant polymorphic ventricular tachycardia have been reported in patients taking raspberry ketone.
Warfarin (Coumadin)
Theoretically, raspberry ketone might increase warfarin dose requirements.
In one case report, a patient taking warfarin 55 mg per week had a decrease in INR over a period of one month while taking raspberry ketone 250 mg daily. A warfarin dose increase to 70 mg per week was necessary to maintain a therapeutic INR while taking raspberry ketone. The mechanism for this potential interaction is not known.
Calcium
Ceftriaxone (Rocephin)
Co-administration of intravenous calcium and ceftriaxone can result in precipitation of a ceftriaxone-calcium salt in the lungs and kidneys.
Avoid administering intravenous calcium in any form, such as parenteral nutrition or Lactated Ringers, within 48 hours of intravenous ceftriaxone. Case reports in neonates show that administering intravenous ceftriaxone and calcium can result in precipitation of a ceftriaxone-calcium salt in the lungs and kidneys. In several cases, neonates have died as a result of this interaction. So far there are no reports in adults; however, there is still concern that this interaction might occur in adults.
Dolutegravir (Tivicay)
Calcium seems to reduce levels of dolutegravir.
Advise patients to take dolutegravir either 2 hours before or 6 hours after taking calcium supplements. Pharmacokinetic research suggests that taking calcium carbonate 1200 mg concomitantly with dolutegravir 50 mg reduces plasma levels of dolutegravir by almost 40%. Calcium appears to decrease levels of dolutegravir through chelation.
Elvitegravir (Vitekta)
Calcium seems to reduce levels of elvitegravir.
Advise patients to take elvitegravir either 2 hours before or 2 hours after taking calcium supplements. Pharmacokinetic research suggests that taking calcium along with elvitegravir can reduce blood levels of elvitegravir through chelation.
Aluminum
Calcium citrate might increase aluminum absorption and toxicity. Other types of calcium do not increase aluminum absorption.
Calcium citrate can increase the absorption of aluminum when taken with aluminum hydroxide. The increase in aluminum levels may become toxic, particularly in individuals with kidney disease. However, the effect of calcium citrate on aluminum absorption is due to the citrate anion rather than calcium cation. Calcium acetate does not appear to increase aluminum absorption.
Bictegravir/Emtricitabine/Tenofovir Alafenamide (Biktarvy)
Calcium might decrease levels of bictegravir/emtricitabine/tenofovir alafenamide by reducing its absorption when taken in a fasting state.
Advise patients that bictegravir/emtricitabine/tenofovir alafenamide and calcium can be taken together if taken with food. However, if taken on an empty stomach, bictegravir/emtricitabine/tenofovir alafenamide should not be taken with, or 2 hours after, calcium containing products.
Bisphosphonates
Calcium reduces the absorption of bisphosphonates.
Advise patients to take bisphosphonates at least 30 minutes before calcium, but preferably at a different time of day. Calcium supplements decrease absorption of bisphosphonates.
Calcipotriene (Dovonex)
Taking calcipotriene with calcium might increase the risk for hypercalcemia.
Calcipotriene is a vitamin D analog used topically for psoriasis. It can be absorbed in sufficient amounts to cause systemic effects, including hypercalcemia. Theoretically, combining calcipotriene with calcium supplements might increase the risk of hypercalcemia.
Digoxin (Lanoxin)
Using intravenous calcium with digoxin might increase the risk of fatal cardiac arrhythmias.
Hypercalcemia increases the risk of fatal cardiac arrhythmias with digoxin. However, one retrospective analysis of clinical data suggests that intravenous calcium does not increase the risk of dysrhythmias or mortality in patients receiving digoxin.
Diltiazem (Cardizem, Others)
Theoretically, calcium may reduce the therapeutic effects of diltiazem.
Hypercalcemia can reduce the effectiveness of verapamil in atrial fibrillation. Theoretically, calcium might increase this risk of hypercalcemia and reduce the effectiveness of diltiazem.
Levothyroxine (Synthroid, Others)
Calcium seems to reduce the absorption and effectiveness of levothyroxine.
Advise patients to take levothyroxine and calcium supplements at least 4 hours apart. Calcium reduces levothyroxine absorption, probably by forming insoluble complexes. Calcium carbonate supplements reduce effectiveness of levothyroxine in patients with hypothyroidism.
Lithium
Theoretically, concomitant use of calcium and lithium may increase this risk of hypercalcemia.
Clinical research suggests that long-term use of lithium may cause hypercalcemia in 10% to 60% of patients. Theoretically, concomitant use of lithium and calcium supplements may further increase this risk.
Quinolone Antibiotics
Calcium seems to reduce the absorption of quinolone antibiotics.
Advise patients to take oral quinolones at least 2 hours before or 4-6 hours after calcium supplements or calcium-fortified foods. Taking calcium at the same time as oral quinolones can reduce quinolone absorption. Calcium binds to quinolones in the gut.
Raltegravir (Isentress)
Calcium may reduce levels of raltegravir.
Pharmacokinetic research shows that taking a single dose of calcium carbonate 3000 mg along with raltegravir 400 mg twice daily modestly decreases the mean area under the curve of raltegravir, but the decrease does not necessitate a dose adjustment of raltegravir. However, a case of elevated HIV-1 RNA levels and documented resistance to raltegravir has been reported for a patient taking calcium carbonate 1 gram three times daily plus vitamin D3 (cholecalciferol) 400 IU three times daily in combination with raltegravir 400 mg twice daily for 11 months. It is thought that calcium reduced raltegravir levels by chelation, leading to treatment failure.
Sotalol (Betapace)
Calcium seems to reduce the absorption of sotalol.
Advise patients to separate doses by at least 2 hours before or 4-6 hours after calcium. Calcium appears to reduce the absorption of sotalol, probably by forming insoluble complexes.
Tetracycline Antibiotics
Calcium seems to reduce the absorption of tetracycline antibiotics.
Advise patients to take oral tetracyclines at least 2 hours before, or 4-6 hours after calcium supplements. Taking calcium at the same time as oral tetracyclines can reduce tetracycline absorption. Calcium binds to tetracyclines in the gut.
Thiazide Diuretics
Taking calcium along with thiazides might increase the risk of hypercalcemia and renal failure.
Thiazides reduce calcium excretion by the kidneys. Using thiazides along with moderately large amounts of calcium carbonate increases the risk of milk-alkali syndrome (hypercalcemia, metabolic alkalosis, renal failure). Patients may need to have their serum calcium levels and/or parathyroid function monitored regularly.
Verapamil (Calan, Others)
Theoretically, calcium may reduce the therapeutic effects of verapamil.
Hypercalcemia can reduce the effectiveness of verapamil in atrial fibrillation. Theoretically, use of calcium supplements may increase this risk of hypercalcemia and reduce the effectiveness of verapamil.
Calcium Channel Blockers
Intravenous calcium may decrease the effects of calcium channel blockers; oral calcium is unlikely to have this effect.
Intravenous calcium is used to decrease the effects of calcium channel blockers in the management of overdose. Intravenous calcium gluconate has been used before intravenous verapamil (Isoptin) to prevent or reduce the hypotensive effects without affecting the antiarrhythmic effects. But there is no evidence that dietary or supplemental calcium when taken orally interacts with calcium channel blockers.
cAMP
Dipyridamole (Persantine)
Dipyridamole can increase the therapeutic and toxic effects of adenosine.
Dipyridamole decreases the metabolism of adenosine. Intravenous infusion of adenosine in patients who are taking dipyridamole can cause dizziness, bradycardia, and syncope. Dipyridamole should be discontinued for several days prior to a cardiac stress test using adenosine.
Carbamazepine (Tegretol)
Carbamazepine might increase the risk of heart block when used concomitantly with adenosine.
Carbamazepine and adenosine can both cause heart block. Giving them concurrently might produce an additive effect.
Methylxanthines
Methylxanthines are competitive antagonists of adenosine and can block its pharmacologic effects.
The methylxanthines, aminophylline, caffeine, and theophylline, can block the effects of adenosine by acting as competitive antagonists at adenosine cell surface receptors. It is recommended that methylxanthines be avoided for 24 hours prior to cardiac stress tests.
Choline Bitartrate
Atropine
Theoretically, choline might decrease the effects of atropine in the brain.
Animal research shows that administering choline one hour before administering atropine can attenuate atropine-induced decreases in brain levels of acetylcholine. Theoretically, concomitant use of choline and atropine may decrease the effects of atropine.
Brand information
Manufacturer and brand details for Amphetalean, from the product label.
Beast
See all Beast products- Name
- BEAST SPORTS NUTRITION
- Street Address
- 7491 NORTH FEDERAL HWY. C5-148
- City
- BOCA RATON
- State
- FL
- ZipCode
- 33487
Amphetalean by Beast: 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 Amphetalean’s Ingredients
Every ingredient we hold a full HelloPharmacist monograph for — uses, evidence, safety, and the complete interaction list.
Niacin
Interacts with 727 drugsNiacin (vitamin B3) is an essential nutrient your body needs for energy and metabolism, and deficiency is uncommon in most developed countries. Prescription-strength niacin has been used to...
Read the full Niacin monograph → Herb & supplement monographCalcium
Interacts with 168 drugsCalcium is an essential mineral your body needs for strong bones, nerve signaling, and muscle function, and supplements can help fill gaps when diet falls short. Most people do best getting...
Read the full Calcium monograph → Herb & supplement monographHordenine
Interacts with 329 drugsHordenine is a natural alkaloid found in barley and some cacti that is marketed as a stimulant for energy, focus, and fat loss, but solid human evidence for these benefits is lacking. Its sa...
Read the full Hordenine monograph → Herb & supplement monographCholine
Interacts with 16 drugsCholine is an essential nutrient your body needs for liver function, brain health, and nerve signaling, and many people get enough from foods like eggs, meat, and fish. Supplements may help...
Read the full Choline monograph → Herb & supplement monographAdenosine
Interacts with 47 drugsAdenosine is a natural building block your body uses for energy and cell signaling, and a prescription injectable version is used by doctors to treat certain fast heart rhythms. As an over-t...
Read the full Adenosine monograph → Herb & supplement monographHigenamine
Interacts with 891 drugsHigenamine is a plant-based stimulant compound added to many weight-loss and pre-workout supplements, but there is very little human evidence that it works and real concerns about heart and...
Read the full Higenamine 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 monographRaspberry Ketone
Interacts with 174 drugsRaspberry ketone is a natural aroma compound found in red raspberries that is heavily marketed for weight loss, but there is no good human evidence that it helps people lose weight. Most cla...
Read the full Raspberry Ketone monograph → Herb & supplement monographEvodia
Interacts with 950 drugsEvodia is a fruit used in traditional Chinese medicine, most often for digestive complaints, headaches, and menstrual pain. Human evidence for these uses is very limited, and it is mostly st...
Read the full Evodia monograph →Sources & How We Checked
Amphetalean'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 283 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.
Niacin 66 references
- Garg R, Malinow MR, Pettinger M, et al. Niacin treatment increases plasma homocysteine levels. Am Heart J 1999;138:1082-7.
- Anon. Inositol hexaniacinate. Altern Med Rev 1998;3:222-3.
- Knodel LC, Talbert RL. Adverse effects of hypolipidaemic drugs. Med Toxicol 1987;2:10-32. PubMed
- Guyton JR, Blazing MA, Hagar J, et al. Extended-release niacin vs gemfibrozil for the treatment of low levels of high-density lipoprotein cholesterol. Niaspan-Gemfibrozil Study Group. Arch Intern Med 2000;160:1177-84. PubMed
- Gibbons LW, Gonzalez V, Gordon N, Grundy S. The prevalence of side effects with regular and sustained-release nicotinic acid. Am J Med 1995;99:378-85. PubMed
- Whelan AM, Price SO, Fowler SF, Hainer BL. The effect of aspirin on niacin-induced cutaneous reactions. J Fam Pract 1992;34:165-8.
- Jungnickel PW, Maloley PA, Vander Tuin EL, et al. Effect of two aspirin pretreatment regimens on niacin-induced cutaneous reactions. J Gen Intern Med 1997;12:591-6. PubMed
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DISCLAIMER: Currently this does not check for drug-drug interactions. This is not an all-inclusive comprehensive list of potential interactions and is for informational purposes only. Not all interactions are known or well-reported in the scientific literature, and new interactions are continually being reported. Input is needed from a qualified healthcare provider including a pharmacist before starting any therapy. Application of clinical judgment is necessary.
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