Beta blockers, such as metoprolol and propranolol. They block beta-adrenergic receptors, lowering heart rate, contractility and blood pressure.

ACE inhibitors, such as lisinopril and enalapril. They block angiotensin-converting enzyme so angiotensin I is not converted to angiotensin II, which lowers blood pressure; a dry cough is the hallmark adverse effect.

Angiotensin II receptor blockers, such as losartan and valsartan. They block angiotensin II at the AT1 receptor, lowering blood pressure without the cough associated with ACE inhibitors.

Dihydropyridine calcium channel blockers, such as amlodipine and nifedipine. They block L-type calcium channels mainly in vascular smooth muscle, producing vasodilation and lower blood pressure.

HMG-CoA reductase inhibitors, such as atorvastatin and simvastatin. They inhibit the rate-limiting enzyme of hepatic cholesterol synthesis, chiefly lowering LDL cholesterol; myopathy is the notable adverse effect. The reserved stem is really -vastatin: nystatin ends in -statin but is an antifungal.

Thiazide diuretics, such as hydrochlorothiazide. They inhibit the sodium-chloride symporter in the distal convoluted tubule, increasing sodium and water excretion; hypokalemia is a common adverse effect.

Loop diuretics, such as furosemide and torsemide. They inhibit the sodium-potassium-two-chloride cotransporter in the thick ascending limb of the loop of Henle, producing powerful diuresis.

Alpha-1 adrenergic blockers, such as prazosin, doxazosin and terazosin. They relax vascular and prostatic smooth muscle, lowering blood pressure and easing urinary flow in benign prostatic hyperplasia; first-dose orthostatic hypotension is characteristic. Tamsulosin is the same class but ends in -osin rather than -zosin, so the short stem does not identify it.

Proton pump inhibitors, such as omeprazole and pantoprazole. They irreversibly inhibit the H+/K+ ATPase of gastric parietal cells, sharply reducing acid secretion.

H2 receptor antagonists, such as famotidine and cimetidine. They block histamine H2 receptors on parietal cells, reducing gastric acid secretion less profoundly than proton pump inhibitors do.

Penicillin-class beta-lactam antibiotics, such as amoxicillin and piperacillin. They inhibit bacterial cell wall synthesis by binding penicillin-binding proteins, and are bactericidal.

Tetracycline antibiotics, such as doxycycline and minocycline. They bind the 30S ribosomal subunit to block bacterial protein synthesis; they can stain developing teeth and cause photosensitivity.

Fluoroquinolone antibiotics, such as ciprofloxacin and levofloxacin. They inhibit bacterial DNA gyrase and topoisomerase IV, and carry a warning for tendinitis and tendon rupture.

Macrolide antibiotics, such as azithromycin, erythromycin and clarithromycin. They bind the 50S ribosomal subunit and inhibit protein synthesis; several are notable inhibitors of hepatic CYP enzymes.

Azole antifungals, such as fluconazole and ketoconazole. They inhibit lanosterol 14-alpha-demethylase, blocking ergosterol synthesis and disrupting the fungal cell membrane.

Antivirals, such as acyclovir, oseltamivir and ritonavir. The longer substems specify the target: -ciclovir agents inhibit viral DNA polymerase, -amivir agents inhibit neuraminidase, and -navir agents inhibit HIV protease.

Benzodiazepines, such as diazepam, lorazepam and alprazolam. They enhance the action of GABA at the GABA-A receptor, producing sedation, anxiolysis and muscle relaxation.

Barbiturates, such as phenobarbital. They also act at the GABA-A receptor, but have a narrower therapeutic window than benzodiazepines and are far more dangerous in overdose.

Serotonin 5-HT1B/1D receptor agonists, such as sumatriptan. They treat acute migraine attacks and cause cranial vasoconstriction, which is why they are avoided in uncontrolled coronary artery disease.

Serotonin 5-HT3 receptor antagonists, such as ondansetron. They are antiemetics used especially for chemotherapy-induced and postoperative nausea and vomiting, and can prolong the QT interval.

Heparin-type anticoagulants, such as heparin and enoxaparin. They potentiate antithrombin III, which then inactivates thrombin and factor Xa; low molecular weight forms act mainly on factor Xa.

Direct factor Xa inhibitors, such as apixaban and rivaroxaban. They block factor Xa directly and, unlike warfarin, do not require routine INR monitoring.

DPP-4 inhibitors, such as sitagliptin. They block DPP-4, prolonging incretin action and increasing glucose-dependent insulin release.

SGLT2 inhibitors, such as empagliflozin. They block glucose reabsorption in the proximal tubule, increasing urinary glucose excretion.

Thiazolidinediones, such as pioglitazone. They are PPAR-gamma agonists that improve peripheral insulin sensitivity.

-mab denotes a monoclonal antibody, a large protein given by injection or infusion. -nib denotes a small-molecule kinase inhibitor, usually taken orally. Both stems are common in oncology and immunology.

Why do generic drug names share suffixes?

Generic names are assigned through the United States Adopted Names and WHO International Nonproprietary Name programs, which reserve a stem for each pharmacologic class. New drugs in a class receive names ending in that stem, so the ending encodes real information about mechanism.

Are drug suffixes always reliable for identifying a class?

Mostly, but not universally. Metronidazole ends in -azole yet is an antibacterial rather than an antifungal, and -mycin appears in macrolides, aminoglycosides and vancomycin, which belong to three different classes. Use the longest stem available, such as -conazole or -thromycin, and memorize the well-known exceptions.

How should I study drug classes for a pharmacology exam?

Learn the stems first so unfamiliar drug names remain classifiable, then attach mechanism, main indication and hallmark adverse effect to each class. Cram can turn pharmacology lecture notes into flashcards with AI and use spaced repetition so the stems stay separated instead of blurring.

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Pharmacology Drug Suffixes flashcards

This deck maps generic drug name stems to their pharmacologic class and mechanism. It covers the cardiovascular stems (-olol, -pril, -sartan, -dipine, -statin, -thiazide, -semide, -zosin), the anti-infective stems (-cillin, -cycline, -floxacin, -thromycin, -conazole, -vir), the gastrointestinal stems (-prazole, -tidine), the central nervous system stems (-azepam, -barbital, -triptan), the endocrine stems (-gliptin, -gliflozin, -glitazone), and the anticoagulant, antiemetic and biologic stems. Each card names the class and states what that class actually does.

Stems are assigned deliberately: the USAN and WHO naming programs reserve an ending for each pharmacologic class, which is why an unfamiliar generic name is often still classifiable on sight. That makes stems worth learning before individual drugs, because exam questions regularly hand you a drug you have never seen and expect you to reason about its class. The deck also flags the stems that are unreliable, since assuming a pattern holds is the classic way to lose the point.

The deck

How to study this deck

Learn each stem as a three-part chain: stem, class, mechanism. '-pril means ACE inhibitor means blocks conversion of angiotensin I to angiotensin II' is recallable under pressure in a way a bare stem-to-class pair is not.
Group the blood-pressure stems and drill them together — -olol, -pril, -sartan, -dipine, -thiazide and -zosin all lower blood pressure by different mechanisms, and questions almost always test the mechanism rather than the effect.
Keep a short exception list beside the deck. Metronidazole ends in -azole but is an antibacterial, duloxetine ends in -oxetine but is an SNRI rather than an SSRI, and -mycin spans three unrelated classes; rehearsing the exceptions is what keeps the rules usable.

Pharmacology Drug Suffixes: FAQ

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