Drug Name Stems & Sulfonamide-Containing Drugs

Reading small-molecule stems

Why stems matter. Generic names are built from standardized stems that encode drug class, so an unfamiliar name in a vignette usually reveals its mechanism and therefore its expected adverse effects.

Class clues. ACE inhibitors cause a bradykinin cough that ARBs avoid. The -dipine calcium channel blockers act mainly on vascular smooth muscle and cause edema and flushing, and statins cause myopathy and raised transaminases. Tamsulosin is an α_1A-selective -osin variant, and α₁-blockers cause first-dose orthostatic hypotension. SGLT2 inhibitors cause glycosuria and genital yeast infections, DPP-4 inhibitors prolong endogenous incretins (GLP-1 and GIP), and GLP-1 agonists cause weight loss and nausea. PPIs irreversibly block the parietal-cell H⁺/K⁺ ATPase. Cimetidine is the -tidine outlier: it inhibits CYP450 and has antiandrogen effects such as gynecomastia.

Mechanism clues. Argatroban and bivalirudin are IV direct thrombin inhibitors without the -gatran stem. Thrombolytics convert plasminogen to plasmin, which lyses fibrin. Nondepolarizing blockers compete with acetylcholine at nicotinic receptors and are reversed by neostigmine or, for rocuronium and vecuronium, by sugammadex. PDE5 inhibitors treat erectile dysfunction and pulmonary hypertension, bisphosphonates inhibit osteoclasts, fluoroquinolones inhibit DNA gyrase and topoisomerase IV, and azoles block ergosterol synthesis.

Do not confuse -triptyline (a tricyclic that blocks amine reuptake) with -triptan (a serotonin receptor agonist that aborts migraine).

Biologic suffixes

Monoclonal antibodies. The ending -mab marks a monoclonal antibody, and the syllable before it traditionally showed how much mouse protein remains: -omab murine (ibritumomab), -ximab chimeric with mouse variable regions (rituximab, infliximab), -zumab humanized with only mouse CDRs (trastuzumab, bevacizumab), and -umab fully human (adalimumab, denosumab). Less mouse sequence means lower immunogenicity and fewer anti-drug antibodies.

• -cept: receptor or ligand domain fused to IgG Fc, as in etanercept (TNF receptor) and abatacept (CTLA-4).
• -nib: small-molecule kinase inhibitor, as in imatinib, erlotinib and tofacitinib.
• -limus: binds FKBP12; tacrolimus then inhibits calcineurin, whereas sirolimus and everolimus inhibit mTOR (cyclosporine instead binds cyclophilin). Sirolimus spares the kidney but impairs wound healing.
• -kinra and -leukin: anakinra is an IL-1 receptor antagonist; aldesleukin is recombinant IL-2.

Sulfonamide-containing drugs

The list. A sulfonamide group appears in many nonantibiotic drugs: probenecid, the loop diuretics furosemide, bumetanide and torsemide, acetazolamide, thiazides, celecoxib, sulfonylureas, sulfasalazine and TMP-SMX; dapsone is a closely related sulfone.

Shared toxicities. Reactions range from rash to Stevens-Johnson syndrome and TEN, and include photosensitivity, oxidant hemolysis in G6PD deficiency, and acute interstitial nephritis. Sulfonamides displace bilirubin from albumin and can cause kernicterus, so antibiotic sulfonamides are avoided near term and in infants younger than 2 months.

Ethacrynic acid is the loop diuretic without a sulfonamide group, the classic choice in severe sulfa allergy, at the cost of greater ototoxicity. Real cross-reactivity between antibiotic and nonantibiotic sulfonamides is low, but exams expect this substitution.