St. John's Wort — Critical Drug Interactions

Critical Drug Interactions — scientific infographic poster

⚠ CRITICAL SAFETY WARNING

St. John's Wort has the most extensive and clinically significant drug-interaction profile of any commonly used medicinal herb. Documented cases include unintended pregnancies in women taking oral contraceptives, acute organ rejection in transplant patients, human immunodeficiency virus (HIV) antiretroviral treatment failure with viral resistance, warfarin anticoagulation failure with thrombotic events, and life-threatening serotonin syndrome from combination with selective serotonin reuptake inhibitors (SSRIs). The U.S. Food and Drug Administration (FDA), European Medicines Agency, Health Canada, the UK Medicines and Healthcare products Regulatory Agency, and Australia's Therapeutic Goods Administration have all issued formal regulatory warnings. The 2022 European Union (EU) herbal monograph states that St. John's Wort preparations supplying more than 1 mg of hyperforin a day speed up the drug-clearing enzymes CYP3A4, CYP2B6, CYP2C9 and CYP2C19 and the drug pump P-glycoprotein. It lists use with coumarin-type blood thinners (such as warfarin), cyclosporine, tacrolimus, sirolimus, everolimus, protease inhibitors and nucleoside reverse transcriptase inhibitors (HIV medicines), irinotecan, imatinib and similar cancer drugs as contraindicated, and states that hormonal contraceptives can become less reliable. The raised enzyme activity returns to normal within about 1 week of stopping, and the monograph notes that interactions with anaesthesia drugs are identified before planned surgery.

The same hyperforin molecule that drives St. John's Wort's antidepressant efficacy also produces its catastrophic drug-interaction profile. Hyperforin is a potent agonist of the pregnane X receptor (PXR), which is the master transcription factor controlling expression of the CYP3A4, CYP1A2, CYP2C9, and CYP2C19 cytochrome P450 enzymes and the P-glycoprotein drug efflux transporter. PXR activation by hyperforin upregulates these drug-metabolizing systems by 50-300% over baseline, dramatically accelerating the clearance of any drug that is a substrate. More than half of all prescription drugs in clinical use are metabolized by cytochrome P450 3A4 (CYP3A4) alone — including oral contraceptives, anticoagulants, immunosuppressants, human immunodeficiency virus antiretrovirals, cardiac drugs, chemotherapy, statins, anticonvulsants, and many psychiatric medications. The clinical consequences range from contraceptive failure (with documented unintended pregnancies) to organ-rejection cases in transplant patients to antiretroviral treatment failure with viral resistance to anticoagulation failure with thrombotic events. Separately, the herb's pharmacodynamic interaction with serotonergic drugs (selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors (SNRIs), triptans, tramadol, monoamine oxidase inhibitors (MAOIs)) can produce potentially fatal serotonin syndrome. This deep-dive walks through the molecular mechanism, the comprehensive interaction tables, the U.S. Food and Drug Administration and international regulatory warning history, and the practical clinical-decision framework for any patient considering or already taking St. John's Wort.

Table of Contents

  1. Molecular Mechanism — PXR Activation by Hyperforin
  2. Comprehensive Cytochrome P450 3A4 Interaction Table
  3. Oral Contraceptives — Documented Contraceptive Failures
  4. Warfarin and Anticoagulants
  5. Immunosuppressants — Organ Rejection Cases
  6. Human Immunodeficiency Virus Antiretrovirals — Contraindicated or Not Recommended
  7. Serotonin Syndrome with Selective Serotonin Reuptake Inhibitors/Serotonin-Norepinephrine Reuptake Inhibitors/Triptans
  8. Cardiac Drugs (Digoxin, Statins, Antiarrhythmics)
  9. Chemotherapy and Targeted Cancer Therapies
  10. Anticonvulsants and Psychiatric Medications
  11. U.S. Food and Drug Administration, European Medicines Agency, and Health Canada Warning History
  12. Surgical and Anesthetic Considerations
  13. Clinical Decision Framework
  14. Key Research Papers
  15. Connections
  16. Featured Videos

Molecular Mechanism — PXR Activation by Hyperforin

The pharmacological root of St. John's Wort's drug-interaction profile is the activation of the pregnane X receptor (PXR) by hyperforin, the herb's principal antidepressant constituent. PXR (also known as NR1I2 or the steroid and xenobiotic receptor SXR) is a nuclear hormone receptor that functions as the master transcription factor controlling expression of the body's xenobiotic metabolism and elimination machinery.

When PXR is activated by an agonist (endogenous bile acids, hyperforin, the antibiotic rifampin, the antifungal clotrimazole, and various other xenobiotics), it translocates to the nucleus, heterodimerizes with the retinoid X receptor (RXR), and binds to PXR response elements (DR3 motifs) in the promoter regions of target genes including:

The induction kinetics matter clinically:

The clinical consequence: any drug whose effective plasma concentration depends on CYP3A4, CYP1A2, CYP2C9, CYP2C19, P-gp, or UGT metabolism will have reduced plasma levels and reduced clinical effect when hypericum is co-administered. The magnitude of the interaction varies by drug (some have plasma level reductions of 25%, others of 75% or more), but the direction is consistent: hypericum reduces drug exposure.

Separately, hyperforin's monoamine reuptake inhibition (the mechanism behind its antidepressant effect) creates a pharmacodynamic interaction with other serotonergic, noradrenergic, and dopaminergic drugs — the effects of those drugs are additive or synergistic with hypericum's. The most clinically dangerous example is serotonin syndrome with selective serotonin reuptake inhibitor (SSRI)/serotonin-norepinephrine reuptake inhibitor (SNRI)/triptan/monoamine oxidase inhibitor (MAOI) combinations.

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Comprehensive Cytochrome P450 3A4 Interaction Table

The following table summarizes the most clinically significant cytochrome P450 3A4-mediated and pharmacodynamic interactions with St. John's Wort. Categories of severity:

Hormonal Contraceptives

Anticoagulants and Antiplatelets

Immunosuppressants (Organ Transplant)

Human Immunodeficiency Virus Antiretrovirals

Cardiovascular Medications

Psychiatric Medications (Pharmacodynamic Serotonin Syndrome Risk)

Chemotherapy and Targeted Cancer Therapies

Anticonvulsants

Other Important Interactions

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Oral Contraceptives — Documented Contraceptive Failures

The hypericum-contraceptive interaction is among the most consequential because the failure mode is a permanent life-altering event (unintended pregnancy) that often occurs without warning — the woman has no way to know contraceptive efficacy is reduced until breakthrough bleeding occurs or, worse, until pregnancy is confirmed.

The mechanism: combined oral contraceptive pills contain ethinyl estradiol (or in newer formulations, estetrol or estradiol valerate) plus a progestin (levonorgestrel, norethindrone, drospirenone, etc.). Both estrogen and progestin components undergo cytochrome P450 3A4 metabolism in the gut wall and liver, and both undergo intestinal P-glycoprotein efflux. Hyperforin's induction of cytochrome P450 3A4 and P-gp accelerates the metabolism and reduces the absorption of both components.

The clinical consequences:

The literature includes multiple case reports and case series of pregnancies in women who became pregnant despite consistent oral contraceptive use after starting hypericum. The German pharmacovigilance database accumulated several documented cases in the late 1990s and early 2000s, which contributed to European Medicines Agency safety communications. The UK Medicines and Healthcare products Regulatory Agency issued a formal warning in 2000. The U.S. Food and Drug Administration followed in 2000 with its first formal hypericum-interaction advisory.

What the guidance and studies describe for women on hormonal contraception who are considering hypericum:

  1. Where pregnancy prevention is essential: the interaction applies to combined oral contraceptive pills, progestin-only pills, the patch, the ring and the etonogestrel implant, and the EU herbal monograph advises any woman using hormonal contraceptives to take additional contraceptive measures
  2. Methods not affected: a copper IUD is not hormonal and is unaffected by enzyme induction, and a levonorgestrel IUD releases its hormone locally, so its interaction risk is lower (breakthrough bleeding may still occur)
  3. Backup methods: the authors of the 2003 pharmacokinetic study concluded that women taking oral contraceptive pills should expect breakthrough bleeding and consider adding a barrier method of contraception (condoms) while taking St. John's Wort; emergency contraception may also be less effective (see the levonorgestrel and ulipristal entries above)
  4. After stopping: the EU herbal monograph states that the raised enzyme activity returns to normal within about 1 week after St. John's Wort is stopped

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Warfarin and Anticoagulants

Warfarin is a vitamin-K-antagonist anticoagulant used for stroke prevention in atrial fibrillation, treatment of venous thromboembolism (deep vein thrombosis and pulmonary embolism), and prevention of clot formation in mechanical heart valves. Therapeutic warfarin dosing requires a delicate balance between adequate anticoagulation (typically targeting an international normalized ratio of 2.0-3.0, or 2.5-3.5 for mechanical valves) and excessive anticoagulation (with bleeding risk).

Hypericum interaction with warfarin:

Management:

Direct oral anticoagulants (DOACs):

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Immunosuppressants — Organ Rejection Cases

Solid organ transplant recipients (kidney, liver, heart, lung, pancreas, small bowel) require lifelong immunosuppression to prevent allograft rejection. Standard regimens typically include a calcineurin inhibitor (cyclosporine or tacrolimus), often combined with mycophenolate and corticosteroids, with maintenance dosing carefully titrated based on therapeutic drug monitoring to keep trough levels within narrow target ranges.

The hypericum-immunosuppressant interaction is among the most catastrophic:

The EU herbal monograph lists use with cyclosporine, tacrolimus, sirolimus and everolimus as contraindicated: hypericum is ABSOLUTELY CONTRAINDICATED in solid organ transplant recipients on these drugs. The interaction has caused documented allograft loss and is not manageable with even intensive therapeutic drug monitoring. Depression after transplantation is usually treated with conventional pharmaceutical antidepressants with known interaction profiles (avoiding strong cytochrome P450 3A4 substrates or inhibitors) or non-pharmaceutical approaches (cognitive behavioral therapy (CBT), exercise, light therapy if seasonal).

Stem cell transplant and hematopoietic cell transplant recipients on immunosuppression for graft-versus-host disease prophylaxis or treatment face the same restrictions.

Patients on biologic immunomodulators (tumor necrosis factor (TNF) inhibitors, JAK inhibitors, IL-17 inhibitors, IL-23 inhibitors) for autoimmune disease generally have lower interaction risk because most biologics are not CYP-metabolized, though interactions differ from agent to agent.

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Human Immunodeficiency Virus Antiretrovirals — Contraindicated or Not Recommended

The hypericum-HIV antiretroviral interaction was the trigger for the first formal U.S. Food and Drug Administration warning about hypericum in February 2000. The seminal study was Piscitelli et al. (Lancet, February 2000), which examined the effect of 14 days of hypericum administration on indinavir pharmacokinetics in healthy volunteers. The results were dramatic:

The clinical consequence: patients on indinavir who add hypericum will experience loss of viral suppression, viral load rebound, and emergence of human immunodeficiency virus protease resistance mutations that may compromise future treatment options. The same magnitude of interaction has been documented with other protease inhibitors and with non-nucleoside reverse transcriptase inhibitors (NNRTIs) including efavirenz and nevirapine.

Integrase strand transfer inhibitors (INSTIs) such as dolutegravir, elvitegravir/cobicistat, raltegravir, and bictegravir are increasingly the first-line antiretroviral class, but they are also significantly affected by hypericum (dolutegravir and bictegravir are UGT substrates that may be affected; cobicistat-boosted regimens lose pharmacokinetic boosting).

The EU herbal monograph lists protease inhibitors and nucleoside reverse transcriptase inhibitors among the combinations it contraindicates, and US drug labels warn against St. John's Wort for most antiretroviral classes — but the label wording differs from drug to drug:

For human immunodeficiency virus-positive patients with depression, antidepressants chosen to fit the antiretroviral regimen commonly include bupropion, mirtazapine, or specific selective serotonin reuptake inhibitors known to have lower cytochrome P450 3A4 interaction (e.g., citalopram or escitalopram, with caution for QT prolongation when combined with certain antiretrovirals).

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Serotonin Syndrome with Selective Serotonin Reuptake Inhibitors/Serotonin-Norepinephrine Reuptake Inhibitors/Triptans

Beyond the pharmacokinetic CYP-induction interactions discussed above, hypericum produces a clinically critical pharmacodynamic interaction with other serotonergic drugs. The mechanism: hyperforin's inhibition of serotonin reuptake (via the TRPC6/sodium-gradient mechanism) adds to the serotonergic effect of pharmaceutical selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors. When combined with other drugs that increase serotonergic signaling (triptans, tramadol, dextromethorphan, MAO inhibitors), the additive effect can produce serotonin syndrome — a potentially fatal hyperthermic crisis.

The clinical features of serotonin syndrome are classified into the Hunter Criteria (the modern diagnostic standard) and include:

Onset is typically within hours to days of adding a second serotonergic agent. The severity ranges from mild (agitation, mild tachycardia, modest tremor) to life-threatening (severe hyperthermia, rigidity, seizures).

Drugs that produce serotonin syndrome risk in combination with hypericum:

Hospital management of suspected serotonin syndrome:

  1. Stopping all serotonergic agents immediately
  2. Supportive care: intravenous (IV) fluids, cooling for hyperthermia, benzodiazepines (lorazepam) for agitation and tremor
  3. Severe cases: intensive care unit (ICU) admission, cyproheptadine (a serotonin 5-HT2A antagonist that may be used as antidote), aggressive cooling, intubation if needed
  4. Most cases resolve within 24-72 hours of stopping serotonergic agents

Serotonin syndrome comes from combining hypericum with another serotonergic medicine: the EU herbal monograph states that St. John's Wort can add to the serotonergic effects of antidepressants such as sertraline and paroxetine, or buspirone, and that serotonin syndrome can very rarely occur. Switches between hypericum and pharmaceutical selective serotonin reuptake inhibitors are usually made with a washout period of at least 2 weeks in either direction (longer for fluoxetine, which has a very long half-life). For more on the cluster of related conditions, see our Depression page.

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Cardiac Drugs (Digoxin, Statins, Antiarrhythmics)

Digoxin: digoxin is a positive inotrope used in heart failure and rate control in atrial fibrillation. It has a narrow therapeutic index (target trough 0.5-2.0 ng/mL) and is primarily a P-glycoprotein substrate (not CYP-metabolized). Hypericum's P-gp induction can reduce digoxin levels by 25-30%, with risk of loss of rate control in atrial fibrillation or worsening heart failure. Co-administration generally avoided; if necessary, digoxin levels monitored closely.

Statins: cholesterol-lowering HMG-CoA reductase inhibitors. Susceptibility to hypericum interaction varies by specific statin:

Calcium channel blockers: most CCBs (amlodipine, nifedipine, felodipine, diltiazem, verapamil) are cytochrome P450 3A4 substrates with reduced antihypertensive effect possible with hypericum co-administration. Blood pressure is monitored if the combination is used.

Antiarrhythmics: amiodarone, quinidine, and dronedarone are cytochrome P450 3A4 substrates with reduced antiarrhythmic effect possible. Amiodarone is particularly problematic because its long half-life means CYP induction effects persist for weeks after hypericum discontinuation.

Ivabradine: a sinus-node funny-current (If) inhibitor used in heart failure; significant cytochrome P450 3A4 substrate with reduced efficacy with hypericum co-administration; clinicians discourage the combination.

Beta-blockers: most beta-blockers have lower cytochrome P450 3A4 dependence and lower interaction risk with hypericum. Carvedilol has some cytochrome P450 2D6 metabolism but is less affected than cytochrome P450 3A4 substrates.

Aspirin and nonsteroidal anti-inflammatory drugs: low interaction risk pharmacokinetically, but combination with hypericum theoretically increases bleeding risk via additive antiplatelet and platelet-function effects (hypericum has weak antiplatelet effect via several mechanisms). Bleeding is watched for if the combination is used.

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Chemotherapy and Targeted Cancer Therapies

Patients on active cancer treatment face particular risk from hypericum interactions because many chemotherapy agents and most targeted molecular therapies are cytochrome P450 3A4 substrates with narrow therapeutic indices. Reduced plasma levels of chemotherapy mean reduced anticancer effect, potentially compromising treatment success.

Specific concerns:

The general principle for cancer patients: the EU herbal monograph lists use with irinotecan, imatinib and other cancer drugs broken down by CYP3A4, CYP2B6, CYP2C9 or CYP2C19 or carried by P-glycoprotein as contraindicated, which covers much of active anticancer treatment. Depression in cancer patients is commonly treated with conventional antidepressants (citalopram, escitalopram, mirtazapine, bupropion) with known interaction profiles. For people in survivorship who are stable on adjuvant therapy, the interaction depends on which adjuvant drug they take (see the table above); people on surveillance alone take no anticancer drug for hypericum to affect.

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Anticonvulsants and Psychiatric Medications

Anticonvulsants used both for seizure disorders and increasingly for mood stabilization (bipolar disorder), neuropathic pain, and migraine prophylaxis have complex interactions with hypericum:

The combination of hypericum with anticonvulsants used for mood stabilization in bipolar disorder is doubly problematic: (1) the pharmacokinetic interaction reduces mood stabilizer effectiveness, and (2) hypericum itself, like other antidepressants, can precipitate manic episodes in bipolar patients. Hypericum is generally contraindicated in bipolar disorder.

Antipsychotic medications:

For any patient on antipsychotic therapy for schizophrenia, schizoaffective disorder, or bipolar disorder, the risk of psychiatric decompensation from sub-therapeutic antipsychotic levels is high and not easily monitored clinically.

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U.S. Food and Drug Administration, European Medicines Agency, and Health Canada Warning History

The international regulatory response to hypericum drug interactions provides important context:

The regulatory warnings have been consistent in their message: St. John's Wort lowers the blood levels of many prescription medicines, and a medicine added while it is being taken can be affected the same way; the EU herbal monograph's list of contraindicated combinations is summarized in the warning box at the top of this page.

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Surgical and Anesthetic Considerations

St. John's Wort interactions with anesthetic and surgical medications create specific perioperative concerns:

The standard recommendation from the American Society of Anesthesiologists and most surgical societies is to discontinue St. John's Wort at least 5 days, ideally 2 weeks, before any planned surgery. The 5-day minimum allows substantial reversal of hyperforin-mediated TRPC6/monoamine effects and partial reversal of cytochrome P450 3A4 induction. The EU herbal monograph states that before elective surgery, interactions with drugs used in general and regional anaesthesia are identified and the herbal product is stopped if necessary, and that the raised enzyme activity returns to normal within 1 week after stopping.

For emergency surgery, the surgical and anesthetic team can adjust drug doses and choices for hypericum only when they know the patient takes it.

Postoperative resumption of hypericum: can typically be resumed once the patient has stabilized postoperatively (1-2 weeks), is off most acute pain medications, and is not on any of the contraindicated postoperative drugs (e.g., warfarin for deep vein thrombosis (DVT) prophylaxis, certain antibiotics, certain analgesics).

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Clinical Decision Framework

For any patient considering St. John's Wort, the following decision framework applies:

  1. Comprehensive medication review: the review covers every prescription medication, every over-the-counter medication, every herbal supplement, every vitamin, and every recreational substance the patient uses. The commercial drug-interaction databases used by pharmacists include hypericum and flag potential interactions
  2. Combinations listed as contraindicated: human immunodeficiency virus antiretrovirals (as detailed above), immunosuppressants in transplant patients, coumarin-type anticoagulants such as warfarin, MAO inhibitors, and much of active chemotherapy. When any of these is present, other depression treatments are used instead
  3. Strongly discouraged combinations: selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, tricyclics, triptans, tramadol, other anticoagulants (DOACs), hormonal contraception in women who depend on it for pregnancy prevention. With any of these, the choice is between moving off the problematic medication and using a different depression treatment
  4. Significant interactions: cardiac medications, statins, anticonvulsants, antipsychotics, calcium channel blockers, theophylline, methadone, sildenafil, etc. These are often manageable with awareness and monitoring
  5. What patients are told: the herb has more drug interactions than any other commonly used supplement; the interactions are real and clinically consequential, not theoretical; a healthcare provider, dentist or pharmacist can check for interactions only when they know it is being taken; any new medication added during hypericum use can be affected; planned surgery includes the interaction check described above; and the antidepressant effect takes about 2 weeks to begin
  6. Monitoring: for patients on warfarin, international normalized ratio every 1-2 weeks initially; for transplant patients (where the combination is contraindicated), trough drug levels; for human immunodeficiency virus patients, viral load monitoring
  7. Discontinuation planning: how long hypericum will be taken, which new medications might be needed in that time, and what happens if an acute illness needs antibiotics or other drug treatment are part of the plan from the start

In practice, the decision often comes down to one question: whether any of the contraindicated or strongly-discouraged medications are present. If they are, the drug-interaction risks described on this page apply in full; other depression options include conventional pharmaceuticals, other herbal antidepressants like saffron, lifestyle approaches, cognitive behavioral therapy and exercise.

For people on no other medications, the 2022 European Union herbal monograph recognizes standardized dry extracts of St. John's Wort (for example 900 mg once a day) as a well-established herbal medicine for the treatment of mild to moderate depressive episodes; people also use hypericum for mood symptoms, mild seasonal affective disorder and menopausal mood symptoms. The interaction profile becomes relevant only when other medications enter the picture.

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Key Research Papers

  1. Piscitelli SC, Burstein AH, Chaitt D, Alfaro RM, Falloon J (2000). Indinavir concentrations and St John's wort. The Lancet, 355(9203):547-8. The pivotal indinavir interaction paper that triggered the FDA warning. — PubMed PMID: 10683007
  2. Moore LB, Goodwin B, Jones SA, Wisely GB, Serabjit-Singh CJ, Willson TM, Collins JL, Kliewer SA (2000). St. John's wort induces hepatic drug metabolism through activation of the pregnane X receptor. PNAS, 97(13):7500-2. The PXR/CYP3A4 mechanism paper. — PubMed: Moore PXR 2000
  3. Markowitz JS, Donovan JL, DeVane CL, Taylor RM, Ruan Y, Wang JS, Chavin KD (2003). Effect of St John's wort on drug metabolism by induction of cytochrome P450 3A4 enzyme. JAMA, 290(11):1500-4. JAMA mechanism paper. — PubMed PMID: 13129991
  4. Henderson L, Yue QY, Bergquist C, Gerden B, Arlett P (2002). St John's wort (Hypericum perforatum): drug interactions and clinical outcomes. British Journal of Clinical Pharmacology, 54(4):349-56. Comprehensive interaction review. — PubMed: Henderson BJCP review
  5. Mannel M (2004). Drug interactions with St John's wort: mechanisms and clinical implications. Drug Safety, 27(11):773-97. Drug Safety review. — PubMed PMID: 15350151
  6. Schwarz UI, Buschel B, Kirch W (2003). Unwanted pregnancy on self-medication with St John's wort despite hormonal contraception. British Journal of Clinical Pharmacology, 55(1):112-3. Documented contraceptive failure case. — PubMed: Schwarz contraceptive failure
  7. Ruschitzka F, Meier PJ, Turina M, Lüscher TF, Noll G (2000). Acute heart transplant rejection due to Saint John's wort. The Lancet, 355(9203):548-9. Documented heart transplant rejection. — PubMed PMID: 10683008
  8. Yue QY, Bergquist C, Gerden B (2000). Safety of St John's wort (Hypericum perforatum). The Lancet, 355(9203):576-7. Swedish pharmacovigilance experience with warfarin and other interactions. — PubMed PMID: 10683030
  9. Lantz MS, Buchalter E, Giambanco V (1999). St. John's wort and antidepressant drug interactions in the elderly. Journal of Geriatric Psychiatry and Neurology, 12(1):7-10. Serotonin syndrome case series. — PubMed: Lantz serotonin syndrome
  10. Hall SD, Wang Z, Huang SM, Hamman MA, Vasavada N, Adigun AQ, Hilligoss JK, Miller M, Gorski JC (2003). The interaction between St John's wort and an oral contraceptive. Clinical Pharmacology and Therapeutics, 74(6):525-35. Detailed pharmacokinetic study of OC interaction. — PubMed PMID: 14663455
  11. Johne A, Brockmöller J, Bauer S, Maurer A, Langheinrich M, Roots I (1999). Pharmacokinetic interaction of digoxin with an herbal extract from St John's wort (Hypericum perforatum). Clinical Pharmacology and Therapeutics, 66(4):338-45. Digoxin interaction characterization. — PubMed: Johne digoxin
  12. Mai I, Bauer S, Perloff ES, Johne A, Uehleke B, Frank B, Budde K, Roots I (2004). Hyperforin content determines the magnitude of the St John's wort-cyclosporine drug interaction. Clinical Pharmacology and Therapeutics, 76(4):330-40. Hyperforin dose-response in cyclosporine interaction. — PubMed PMID: 15470332

PubMed Topic Searches

  1. PubMed: Hypericum CYP3A4 induction
  2. PubMed: Hypericum oral contraceptive failure
  3. PubMed: Hypericum warfarin INR
  4. PubMed: Hypericum transplant rejection
  5. PubMed: Hypericum serotonin syndrome
  6. PubMed: Hyperforin PXR mechanism
  7. PubMed: Hypericum HIV antiretroviral

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Connections

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