1Inhibition and induction side by side
≠ marks rows where the two differ.
| Feature | Inhibitor added | Inducer added |
|---|---|---|
| Differs: Mechanism | Blocks the enzyme that clears the substrate | Increases synthesis of new enzyme protein |
| Differs: Onset | Hours to days, as the inhibitor reaches its own steady state | Roughly 1 to 2 weeks, while new enzyme is made |
| Differs: Offset after stopping | Days, following the inhibitor’s own half-life | Roughly 1 to 2 weeks, while the extra enzyme is cleared |
| Differs: Active substrate | Exposure rises: toxicity risk | Exposure falls: loss of effect |
| Differs: Prodrug activated by the enzyme | Less active drug formed: loss of effect | More active drug formed |
| Differs: FDA strength scale | Strong: AUC of a sensitive substrate up 5-fold or more; moderate: 2- to under 5-fold; weak: 1.25- to under 2-fold | Strong: AUC down 80% or more; moderate: 50% to under 80%; weak: 20% to under 50% |
Strength definitions from the FDA table of drugs that interact with CYP enzymes and transporters. The 1-to-2-week induction timing follows product labeling, with rifampin as the standard example.
2An inducer course, week by week
Day 1
Inducer starts
Substrate levels have barely moved. A level drawn now looks reassuring and predicts nothing.
Weeks 1 to 2
Induction builds
Exposure slides toward a lower plateau. Loss of effect shows up here, often after the patient has left the clinic.
While induced
Compensating dose
If the substrate dose was raised to hold its effect, that higher dose is correct only for as long as induction lasts.
Inducer stops
Enzyme still high
Nothing visible happens for several days, which is exactly why the hazard gets missed.
1 to 2 weeks later
Induction fades
Exposure climbs back while the raised dose is still in place. For a narrow-therapeutic-index drug, this is the toxicity window.
3Reading the label and the FDA table
Interactions are one line of Domain 2, therapeutics and patient management, and the reference that settles most of them is free. The FDA keeps a public table of clinically studied CYP and transporter interactions, sorted by enzyme and strength. A few entries are worth knowing without looking:
- Strong CYP3A inhibitors: clarithromycin, itraconazole, ketoconazole, lopinavir/ritonavir.
- Moderate CYP3A inhibitors: diltiazem, erythromycin, verapamil and grapefruit juice, whose effect the FDA notes varies widely by brand, concentration and preparation.
- Strong CYP3A inducers: carbamazepine, phenytoin, rifampin.
- Strong CYP2D6 inhibitors: bupropion, fluoxetine, paroxetine, quinidine, terbinafine. Strong CYP1A2 inhibitor: fluvoxamine.
Strength alone does not predict harm. A moderate inhibitor matters far more for a sensitive substrate with a narrow therapeutic index than for a drug with a wide margin, and the substrate’s own label usually names the action: avoid the pair, adjust the dose, or monitor.
3.1When the direction flips
For a prodrug that needs the enzyme to become active, everything reverses: an inhibitor lowers the active drug and an inducer raises it. Read whether the parent or the metabolite does the work before deciding which way the interaction runs.
CYP450 is also only part of the picture. Glucuronidation (UGT) and transporters such as P-glycoprotein are induced and inhibited too, and labels list those effects in the same drug interactions section.
4Before you answer an interaction case
- Name the enzyme or transporter, and decide whether the newcomer inhibits or induces it.
- Check whether the affected drug is active as given or a prodrug.
- Place the case on the clock: the interacting drug is starting, steady, or stopping.
- Ask how narrow the affected drug’s margin is and whether a level or lab marker can track it.
- Read the label’s own instruction for the pair: avoid, adjust or monitor.
- Time the follow-up for when the change peaks, which for induction is weeks away.
5Drug pairs on the clock
The pairs below sit at different points on that clock. Settle which way exposure moves, and how soon, then commit to a plan.
Study cases written by our editors, not BPS items. The real BCPS exam is computer-based multiple choice, answered in order with no going back.
Case 1 of 9 · 0 answered
How case rounds work
Pick an option to see the verdict and a note on every option. Keys while the round has focus: 1–5 or A–E answer, ← → move between cases. Nothing is saved or sent anywhere.
Case 01
A 38-year-old man with HIV (CD4 180 cells/mm³, viral load undetectable) on bictegravir/tenofovir alafenamide/emtricitabine is diagnosed with drug-susceptible pulmonary tuberculosis. Rifampin-based therapy (RIPE) is planned. SCr is 0.9 mg/dL. Which plan is most appropriate?
Pick an option: the verdict and a note on every option open here.
Best answer: A.
Rifampin strongly induces UGT1A1 and CYP3A4 and is contraindicated with bictegravir (and not recommended with TAF), so ART is changed to dolutegravir increased to 50 mg twice daily with TDF/FTC for the duration of rifampin and 2 weeks after. Rifabutin is the usual fix for protease inhibitor regimens, but coadministration with bictegravir is also not recommended. Continuing BIC/TAF/FTC unchanged produces subtherapeutic levels and resistance, and stopping effective ART during TB treatment raises mortality.
- A
- Correct. Bictegravir cannot be given with rifampin, so ART switches to dolutegravir 50 mg twice daily with TDF/FTC during RIPE.
- B
- Rifampin sharply lowers bictegravir and TAF levels, which leads to virologic failure and resistance.
- C
- Stopping effective ART during TB treatment raises mortality, especially with a CD4 of 180.
- D
- Rifabutin solves the problem for protease inhibitors, but it is not recommended with bictegravir either.
Case 02
A 48-year-old kidney transplant recipient takes tacrolimus 4 mg twice daily (trough 8 ng/mL; goal 6–10 ng/mL) with mycophenolate and prednisone. Fluconazole 200 mg daily was started 5 days ago for esophageal candidiasis. Today he has a hand tremor, his tacrolimus trough is 17 ng/mL, and SCr has risen from 1.2 to 1.7 mg/dL. Which action is most appropriate?
Pick an option: the verdict and a note on every option open here.
Best answer: C.
Fluconazole inhibits CYP3A4 and raises tacrolimus exposure, and the high trough with tremor and rising creatinine indicates calcineurin-inhibitor toxicity, so the dose should be reduced with a repeat trough in a few days (and increased again when the azole stops). Waiting for the course to end allows ongoing nephrotoxicity. Diltiazem is another CYP3A4 inhibitor that would raise levels further, and stopping tacrolimus risks acute rejection.
- A
- Stopping tacrolimus risks acute rejection, and doubling mycophenolate does not replace calcineurin inhibition.
- B
- Waiting out the fluconazole course lets nephrotoxicity continue for days.
- C
- Correct. Fluconazole inhibits CYP3A4 and doubled the trough; a lower dose and a recheck in 2–3 days correct the toxicity.
- D
- Diltiazem is another CYP3A4 inhibitor and would push tacrolimus higher still.
Case 03
A 73-year-old man with atrial fibrillation has had a stable INR of 2.4 on warfarin 5 mg daily for 6 months. His cardiologist starts amiodarone 400 mg twice daily for 2 weeks, then 200 mg daily, for rhythm control; he cannot take a DOAC because of a mechanical mitral valve. Which plan is most appropriate?
Pick an option: the verdict and a note on every option open here.
Best answer: C.
Amiodarone inhibits CYP2C9 and CYP3A4, so warfarin exposure rises over several weeks; a proactive dose reduction of about 25–50% with at least weekly INR checks until stable prevents over-anticoagulation. Waiting 4 weeks misses the rise, which typically appears in the first 1–4 weeks. Amiodarone is an inhibitor, not an inducer, and a 2-day hold followed by the same dose leaves the interaction unaddressed.
- A
- Amiodarone is an enzyme inhibitor, not an inducer, so INR rises rather than falls.
- B
- A 2-day hold and the same dose afterward leave the ongoing interaction unaddressed.
- C
- Correct. Amiodarone inhibits CYP2C9 and CYP3A4, so a proactive cut of about 25–50% with weekly INRs prevents over-anticoagulation.
- D
- The INR rise usually appears within 1–4 weeks, so a check at 4 weeks comes too late.
Case 04
A 26-year-old woman with focal epilepsy has been seizure-free on carbamazepine ER 600 mg twice daily for a year. She has used a combined oral contraceptive (ethinyl estradiol 30 mcg/levonorgestrel 150 mcg) for 6 months and does not want pregnancy for several years. Which contraceptive counseling is most appropriate?
Pick an option: the verdict and a note on every option open here.
Best answer: A.
Carbamazepine induces CYP3A4 and markedly lowers ethinyl estradiol and progestin levels, so combined and progestin-only pills are unreliable (CDC MEC category 3); an IUD (copper or levonorgestrel) or depot medroxyprogesterone is unaffected and preferred. Consistent timing does not overcome enzyme induction. Doubling pill doses is an outdated, unreliable workaround that is no longer recommended.
- A
- Correct. Carbamazepine is a strong inducer that makes pills unreliable, and an IUD (copper or levonorgestrel) is unaffected.
- B
- Dose timing cannot overcome enzyme induction that lowers both hormone levels.
- C
- A progestin-only pill is affected by the same induction and is just as unreliable.
- D
- Doubling up pills is an outdated, unreliable workaround that is no longer recommended.
Case 05
A 55-year-old man with a mechanical mitral valve takes warfarin (INR goal 3.0, stable). He has latent TB infection after a positive IGRA and a normal chest x-ray. LFTs are normal, he does not drink alcohol, and he has no HIV. Which LTBI regimen is most appropriate?
Pick an option: the verdict and a note on every option open here.
Best answer: D.
Rifamycin-based regimens are usually preferred for LTBI, but rifampin and rifapentine are strong CYP inducers that can drop warfarin’s effect dramatically and make a high-target INR for a mechanical valve nearly impossible to maintain, so CDC lists isoniazid (6–9 months, with pyridoxine) as the alternative when interactions preclude a rifamycin. Four months of rifampin and weekly 3HP both carry the induction problem. Rifampin plus pyrazinamide is no longer recommended because of severe hepatotoxicity.
- A
- Weekly 3HP still contains rifapentine, a strong inducer that would undercut his warfarin control.
- B
- Rifampin is a potent CYP inducer that would make a high-target INR for a mechanical valve very hard to hold.
- C
- Rifampin plus pyrazinamide for 2 months is no longer recommended because of severe hepatotoxicity.
- D
- Correct. Rifamycins would wreck his INR control, so isoniazid with pyridoxine is the CDC alternative when interactions rule them out.
Case 06
A 30-year-old man with generalized epilepsy has partial seizure control on valproic acid 1,000 mg daily. His neurologist adds lamotrigine. He takes no other medications. Which initial lamotrigine titration is most appropriate?
Pick an option: the verdict and a note on every option open here.
Best answer: D.
Valproate inhibits lamotrigine glucuronidation and roughly doubles its half-life, so the label requires the slowest titration (25 mg every other day for weeks 1–2, then 25 mg daily for weeks 3–4) to limit the risk of Stevens-Johnson syndrome. The 25-then-50 mg schedule is for patients not taking valproate or enzyme inducers, and the 50-then-100 mg schedule is for patients on inducers such as carbamazepine. Starting at 100 mg greatly raises the risk of serious rash.
- A
- Starting at 100 mg sharply raises the risk of Stevens-Johnson syndrome, especially with valproate on board.
- B
- This is the titration for patients on neither valproate nor an enzyme inducer.
- C
- This faster schedule is meant for patients on enzyme inducers such as carbamazepine.
- D
- Correct. Valproate roughly doubles lamotrigine’s half-life, so the slowest label titration is used to limit serious rash.
Case 07
A 61-year-old woman with a stable INR of 2.5 on warfarin 5 mg daily presents a new prescription for trimethoprim-sulfamethoxazole DS twice daily for 3 days for uncomplicated cystitis. Her CrCl is 80 mL/min, and the prescriber is reachable by phone. Which action by the pharmacist is most appropriate?
Pick an option: the verdict and a note on every option open here.
Best answer: A.
TMP-SMX inhibits CYP2C9 warfarin metabolism and sharply raises the INR within days, so asking for a non-interacting first-line agent such as nitrofurantoin (CrCl above 30 mL/min) prevents the harm. An INR check in 2 weeks comes after the interaction has peaked, and counseling about bleeding alone accepts a preventable risk. Changing the warfarin dose without a prescriber order or a collaborative practice agreement is outside the pharmacist’s authority.
- A
- Correct. TMP-SMX inhibits warfarin metabolism and sharply raises the INR; nitrofurantoin treats cystitis without that interaction.
- B
- Counseling alone accepts a preventable bleeding risk when a safe alternative is one phone call away.
- C
- By 2 weeks the INR rise has already peaked, so the check comes after the harm.
- D
- Changing the warfarin dose without an order or a collaborative practice agreement is outside the pharmacist’s authority.
Case 08
A 64-year-old man with type 2 diabetes takes simvastatin 40 mg each evening (LDL-C 92 mg/dL) and drinks a large glass of grapefruit juice every morning, which he says he will not give up. He has no ASCVD, and CrCl is 80 mL/min. Which recommendation is most appropriate?
Pick an option: the verdict and a note on every option open here.
Best answer: A.
Grapefruit irreversibly inactivates intestinal CYP3A4, sharply raising exposure to simvastatin and lovastatin and with it the risk of myopathy; rosuvastatin is not a CYP3A4 substrate and gives at least equivalent moderate-intensity LDL lowering. Separating the doses by 12 hours does not help because enzyme inactivation persists for 24–72 hours until new enzyme is made. Lovastatin shares the same interaction, and cutting simvastatin to 20 mg lowers efficacy while the interaction persists.
- A
- Correct. Rosuvastatin is not a CYP3A4 substrate, so grapefruit does not raise its levels, and 10 mg gives at least equal LDL lowering.
- B
- Grapefruit inactivates gut CYP3A4 for 24–72 hours, so spacing the doses does not prevent the interaction.
- C
- Lovastatin is a CYP3A4 substrate too and has the same grapefruit interaction.
- D
- A lower simvastatin dose loses efficacy while the interaction remains.
Case 09
A 62-year-old man takes warfarin for a mechanical aortic valve (INR goal 2.5, stable for 6 months). He plans to start several supplements he read about online. Which counseling statement is most accurate?
Pick an option: the verdict and a note on every option open here.
Best answer: B.
St. John’s wort induces CYP2C9, CYP3A4, and P-glycoprotein, lowering warfarin levels and INR—dangerous with a mechanical valve. Ginkgo inhibits platelet-activating factor and adds bleeding risk. Vitamin K intake should be kept consistent rather than eliminated, and fish oil at this dose does not lower the INR (if anything it may slightly increase bleeding tendency).
- A
- Fish oil at this dose does not lower the INR; if anything it slightly adds to bleeding tendency.
- B
- Correct. St. John’s wort induces CYP2C9, CYP3A4 and P-glycoprotein, lowering warfarin levels, which is dangerous with a mechanical valve.
- C
- Ginkgo has antiplatelet effects and adds bleeding risk on warfarin.
- D
- Vitamin K intake should stay consistent, not be eliminated; erratic avoidance destabilizes the INR.
6References
- FDA: Examples of drugs that interact with CYP enzymes and transporter systems. Strength definitions and clinical examples by enzyme. As of October 27, 2026.
- DailyMed: current US product labels. Section 7 of each label (drug interactions) gives the manufacturer’s management advice. As of October 27, 2026.
Next step
Check yourself, then check the notes
Read the note on every option, then decide where the next session goes.
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