Meds MOA

Respiratory (common drugs — indication → MOA)

• Albuterol / Salbutamol (SABA) — reliever for asthma/COPD exacerbations → β₂-adrenergic receptor agonist → bronchodilation via increased cAMP in airway smooth muscle.

• Levalbuterol — same indications → R-enantiomer of albuterol; β₂-agonist.

• Salmeterol / Formoterol (LABA) — long-term control of asthma/COPD → long-acting β₂-agonists producing sustained bronchodilation.

• Ipratropium (SAMA) — COPD/asthma adjunct reliever → muscarinic (M3) receptor antagonist → reduces bronchoconstriction.

• Tiotropium (LAMA) — maintenance COPD/asthma adjunct → long-acting muscarinic antagonist.

• Inhaled corticosteroids (e.g., budesonide, fluticasone) — controller therapy for asthma → reduce airway inflammation via glucocorticoid receptor-mediated gene transcription changes.

• Montelukast / Zafirlukast (leukotriene receptor antagonists) — allergic asthma, exercise-induced bronchospasm → block cysteinyl leukotriene (CysLT) receptors → reduce bronchoconstriction/inflammation.

• Theophylline — (less used) COPD/asthma add-on → phosphodiesterase inhibition → ↑cAMP/bronchodilation; adenosine receptor antagonism.

• Omalizumab — moderate–severe allergic asthma (IgE-driven) → anti-IgE monoclonal antibody → prevents IgE binding to receptors.

• Mepolizumab / Reslizumab (anti-IL-5) — eosinophilic asthma → monoclonal antibodies against IL-5 → reduce eosinophil activation/survival.

• Roflumilast — severe COPD with chronic bronchitis → selective PDE4 inhibitor → reduces inflammation.

Cardiac / Antihypertensive (common drugs — indication → MOA)

• ACE inhibitors (eg, lisinopril, enalapril) — HTN, HF, post-MI, nephropathy → inhibit angiotensin-converting enzyme → ↓Ang II → vasodilation, ↓aldosterone.

• ARBs (eg, losartan, valsartan) — HTN, HF → block AT₁ receptor → similar end effects to ACEIs but no bradykinin increase.

• Beta-blockers (eg, metoprolol, carvedilol, atenolol) — HTN, angina, arrhythmia, heart failure (select drugs) → antagonize β₁/β₂ receptors → ↓HR, contractility, and sympathetic drive.

• Calcium channel blockers (DHP: amlodipine; non-DHP: verapamil, diltiazem) — HTN, angina, rate control → inhibit L-type Ca²⁺ channels → vasodilation (DHP) or ↓AV nodal conduction (non-DHP).

• Diuretics:

  • Thiazides (e.g., hydrochlorothiazide) — HTN, edema → inhibit Na⁺/Cl⁻ transporter in DCT → natriuresis.

  • Loop (e.g., furosemide, bumetanide) — edema, acute pulmonary edema → inhibit NKCC2 in thick ascending limb → potent diuresis.

  • K⁺-sparing (spironolactone, eplerenone; amiloride, triamterene) — HF, hyperaldosteronism → aldosterone antagonists or ENaC blockers.

• Hydralazine — severe HTN, HF (with nitrates) → direct arteriolar vasodilator (vascular smooth muscle relaxation).

• Nitrates (nitroglycerin, isosorbide dinitrate) — angina → NO donor → ↑cGMP → venodilation (↓preload) and some coronary vasodilation.

• Digoxin — systolic HF (rate control in AF) → inhibits Na⁺/K⁺ ATPase → ↑intracellular Ca²⁺ → positive inotropy; vagomimetic effect slows AV conduction.

• Statins (eg, atorvastatin) — hyperlipidemia, ASCVD prevention → inhibit HMG-CoA reductase → ↓cholesterol synthesis, upregulate LDL receptors.

• Antiplatelet/anticoagulants (see vascular/antithrombotic section)

Neuro / Neurology (common drugs — indication → MOA)

• Levodopa + carbidopa — Parkinson disease motor symptoms → levodopa is dopamine precursor; carbidopa inhibits peripheral dopa decarboxylase to increase CNS availability.

• Dopamine agonists (pramipexole, ropinirole) — Parkinson’s → directly stimulate dopamine receptors (D2 agonists).

• Antiepileptics (representative):

  • Phenytoin — focal and generalized tonic-clonic seizures → blocks voltage-gated Na⁺ channels (use-dependent).

  • Carbamazepine — focal seizures, trigeminal neuralgia → Na⁺ channel blocker.

  • Valproate — generalized seizures, bipolar → multiple: ↑GABA, Na⁺ channel inhibition, T-type Ca²⁺ block.

  • Levetiracetam — adjunct in many seizure types → binds SV2A synaptic vesicle protein (modulates neurotransmitter release).

  • Lamotrigine — focal & generalized seizures, bipolar → Na⁺ channel blocker; inhibits glutamate release.

• Benzodiazepines (diazepam, lorazepam) — acute seizures, anxiety → GABA_A receptor positive allosteric modulators → ↑Cl⁻ influx/hyperpolarization.

• Opioids (morphine, fentanyl) — severe pain → μ-opioid receptor agonists → inhibit ascending pain pathways, alter perception.

• Migraine agents:

  • Triptans (sumatriptan) — acute migraine → 5-HT₁B/1D agonists → cranial vasoconstriction + inhibit trigeminal neurotransmission.

  • Topiramate, propranolol — migraine prophylaxis → multiple MOAs (topiramate: Na⁺ channels, GABA ↑; propranolol: β-blockade).

• Acetylcholinesterase inhibitors (donepezil, rivastigmine) — Alzheimer’s symptomatic therapy → inhibit acetylcholinesterase → ↑ACh at synapses.

Gastrointestinal (GI) meds (common drugs — indication → MOA)

• Proton pump inhibitors (omeprazole, pantoprazole, esomeprazole) — GERD, peptic ulcer, Zollinger-Ellison → irreversible H⁺/K⁺-ATPase inhibition in parietal cells → ↓acid secretion.

• H2 blockers (ranitidine [withdrawn in many places], famotidine) — peptic disease, GERD → H₂ receptor antagonists → ↓histamine-mediated acid secretion.

• Antacids (MgOH, AlOH, CaCO₃) — symptomatic heartburn → neutralize gastric acid chemically.

• Sucralfate — stress ulcers, mucosal protection → forms viscous adhesive barrier on ulcer sites.

• Bismuth subsalicylate — diarrhea, H. pylori regimens adjunct → topical GI mucosal effect; antimicrobial effects.

• Laxatives: osmotic (PEG), stimulant (senna), bulk-forming (psyllium) → various mechanisms (water retention, peristalsis stimulation, fiber bulking).

• Antiemetics:

  • Ondansetron — chemo/N/V → 5-HT₃ receptor antagonist.

  • Metoclopramide — gastroparesis, antiemetic → D₂ antagonist + prokinetic via 5-HT₄ agonism.

Endocrine (common drugs — indication → MOA)

• Insulins (rapid: lispro/aspart; short: regular; intermediate: NPH; long: glargine/detemir/degludec) — T1DM & many T2DM cases → exogenous insulin binds insulin receptor (RTK) → ↑glucose uptake/glycogen synthesis, ↓gluconeogenesis.

• Metformin — first-line T2DM → decreases hepatic gluconeogenesis, improves peripheral insulin sensitivity (AMPK activation contribution).

• Sulfonylureas (glipizide, glyburide) — T2DM → close pancreatic β-cell K_ATP channels → insulin release.

• GLP-1 receptor agonists (exenatide, liraglutide) — T2DM, weight loss adjunct → incretin mimetics → ↑glucose-dependent insulin secretion, ↓glucagon, slow gastric emptying.

• DPP-4 inhibitors (sitagliptin) — T2DM → inhibit DPP-4 → ↑endogenous GLP-1 levels.

• SGLT2 inhibitors (empagliflozin, canagliflozin) — T2DM, HF benefits → inhibit renal SGLT2 → ↑glycosuria → lower glucose and mild diuresis.

• Levothyroxine (T4) — hypothyroidism → synthetic thyroxine → replaces thyroid hormone.

• Antithyroid (methimazole, propylthiouracil) — hyperthyroidism → inhibit thyroid peroxidase (and PTU also reduces peripheral T4→T3 conversion).

• Oral corticosteroids (prednisone) — many endocrine/immunologic indications → glucocorticoid receptor agonists altering gene transcription.

Vascular / Antithrombotic (common meds — indication → MOA)

• Aspirin (low dose) — arterial thrombosis prevention → COX-1 irreversible inhibition in platelets → ↓TXA₂ → reduced platelet aggregation.

• P2Y12 inhibitors (clopidogrel, prasugrel, ticagrelor) — ACS, stent → inhibit platelet P2Y12 ADP receptor → prevent platelet activation/aggregation.

• Heparin (UFH) & LMWH (enoxaparin) — VTE prophylaxis/tx, ACS → potentiate antithrombin → inhibit thrombin (IIa) and Xa (LMWH mainly Xa).

• Warfarin — chronic anticoagulation (VTE, A-fib) → inhibits vitamin K epoxide reductase → ↓γ-carboxylation of factors II, VII, IX, X.

• Direct oral anticoagulants (DOACs):

  • Dabigatran — direct thrombin inhibitor (IIa).

  • Rivaroxaban / Apixaban / Edoxaban — direct factor Xa inhibitors.

• Thrombolytics (alteplase) — acute MI, ischemic stroke (selected) → recombinant tPA → converts plasminogen to plasmin → fibrinolysis.

Antibiotics (common classes with typical indications → MOA)

• Penicillins (penicillin G/V, amoxicillin) — many Gram-positive infections, some Gram-negative → inhibit transpeptidase (PBPs) → block cell-wall peptidoglycan crosslinking (bactericidal).

• Beta-lactam + β-lactamase inhibitors (amoxicillin/clavulanate) — extend spectrum vs β-lactamase producers → same cell-wall MOA.

• Cephalosporins (cefazolin, ceftriaxone, cefepime) — broad spectrum depending on generation → inhibit cell-wall synthesis (PBPs).

• Carbapenems (meropenem) — serious multidrug infections → inhibit cell-wall synthesis (broadest β-lactams).

• Macrolides (azithromycin, erythromycin) — atypical pneumonia, STIs → bind 50S ribosomal subunit → inhibit protein synthesis (bacteriostatic/cidal concentration-dependent).

• Tetracyclines (doxycycline) — acne, tick-borne, atypicals → bind 30S ribosomal subunit → block tRNA attachment (bacteriostatic).

• Aminoglycosides (gentamicin, tobramycin) — severe Gram-negative infections (with β-lactam) → bind 30S → cause misreading and inhibit initiation (bactericidal, oxygen-dependent uptake).

• Fluoroquinolones (ciprofloxacin, levofloxacin) — broad Gram-negative/atypical coverage → inhibit DNA gyrase (topo II) and topoisomerase IV → impair DNA replication.

• Vancomycin — MRSA, serious Gram-positive infections → binds D-Ala-D-Ala → inhibits cell-wall peptidoglycan polymerization (bactericidal).

• Metronidazole — anaerobic infections, C. difficile → nitroimidazole reduced in anaerobes → DNA strand breakage.

• Linezolid — VRE, MRSA alternatives → binds 50S subunit at the initiation complex → prevents protein synthesis.

Psychiatric medications (common classes/drugs — indication → MOA)

• SSRIs (fluoxetine, sertraline, citalopram, escitalopram, paroxetine) — depression, anxiety, OCD, PTSD → inhibit serotonin reuptake transporter (SERT) → ↑synaptic 5-HT.

• SNRIs (venlafaxine, duloxetine) — depression, neuropathic pain, anxiety → inhibit serotonin and norepinephrine reuptake transporters.

• TCAs (amitriptyline, nortriptyline) — depression, neuropathic pain → inhibit reuptake of 5-HT and NE; block many other receptors (anticholinergic, antihistamine).

• MAO inhibitors (phenelzine, tranylcypromine) — atypical depression (rare use) → inhibit monoamine oxidase → ↑NE, 5-HT, dopamine (risk of tyramine interactions).

• Atypical antipsychotics (risperidone, olanzapine, quetiapine, clozapine) — schizophrenia, bipolar → D₂ (and variable 5-HT₂A) receptor antagonism/partial agonism; clozapine reserved for refractory schizophrenia.

• Typical antipsychotics (haloperidol)-psychosis, acute agitation → D₂ receptor antagonists.

• Mood stabilizers:

  • Lithium--bipolar disorder maintenance → multiple proposed MOAs (modulates second-messenger systems, inositol monophosphatase inhibition).

  • Valproate-- bipolar mania → increases GABA, modulates Na⁺ channels.

• Benzodiazepines (alprazolam, lorazepam)- acute anxiety, insomnia, seizures → GABA_A positive allosteric modulation.

• Buspirone-generalized anxiety → 5-HT1A partial agonist (non-benzodiazepine anxiolytic).