Pharmacology Reference

ProAir, Proventil, Ventolin, AccuNeb

Selective beta-2 adrenergic agonist. Activates adenylyl cyclase → increases cAMP → smooth muscle relaxation and bronchodilation. Also stabilizes mast cells.

Xopenex

Pure R-enantiomer of racemic albuterol. Binds beta-2 receptors with greater affinity than the S-isomer. S-isomer (in racemic albuterol) may contribute to some adverse effects. Bronchodilation via cAMP-mediated smooth muscle relaxation.

Atrovent

Quaternary ammonium anticholinergic (antimuscarinic). Blocks muscarinic M3 receptors in airway smooth muscle → prevents acetylcholine-mediated bronchoconstriction. Also reduces mucus secretion.

Spiriva

Long-acting muscarinic antagonist (LAMA). Dissociates very slowly from M1 and M3 receptors, providing prolonged bronchodilation. Blocks parasympathetic bronchoconstriction and reduces mucus hypersecretion.

Serevent Diskus

Long-acting selective beta-2 adrenergic agonist. Long lipophilic side chain anchors it to cell membrane near receptor, allowing sustained receptor activation. Increases cAMP → bronchial smooth muscle relaxation.

Foradil, Perforomist, Symbicort (with budesonide)

Long-acting selective beta-2 agonist. Faster onset than salmeterol due to partial hydrophilicity. Activates adenylyl cyclase → cAMP → airway smooth muscle relaxation.

DuoNeb, Combivent Respimat

Combination of beta-2 agonist (albuterol) and anticholinergic (ipratropium). Dual bronchodilation via complementary mechanisms: albuterol relaxes smooth muscle via cAMP; ipratropium blocks muscarinic bronchoconstriction.

Pulmicort, Rhinocort, Symbicort (with formoterol), QVAR (beclomethasone — different)

Synthetic glucocorticoid. Binds intracellular glucocorticoid receptors → nuclear translocation → reduces transcription of inflammatory genes (cytokines, chemokines). Decreases airway eosinophilia, mast cell activity, and mucus production.

Flovent, Flonase, Advair (with salmeterol), Breo (with vilanterol)

High-potency synthetic glucocorticoid. High receptor binding affinity (approximately 3× beclomethasone). Reduces airway inflammation via glucocorticoid receptor-mediated gene regulation.

Solu-Medrol, Medrol (oral)

Synthetic glucocorticoid. Binds cytoplasmic glucocorticoid receptors → nuclear translocation → modifies transcription. Anti-inflammatory: reduces cytokine production, leukocyte migration, vascular permeability. Relative potency: 5× cortisol.

Deltasone, Rayos

Oral glucocorticoid prodrug, converted to active prednisolone in liver. Same mechanism as methylprednisolone. Potency: 4× cortisol.

Decadron, Dexasone

Potent synthetic glucocorticoid with no mineralocorticoid activity. 25–30× potency of cortisol. Penetrates CNS well. Long duration of action. Reduces inflammation and edema.

Mucomyst, Acetadote (IV)

Free thiol group cleaves disulfide bonds in mucus glycoproteins → reduces mucus viscosity. As antidote: replenishes glutathione stores → prevents hepatotoxicity from NAPQI (acetaminophen toxic metabolite).

Pulmozyme

Recombinant human DNase I enzyme. Cleaves extracellular DNA (from neutrophil breakdown) that contributes to the viscosity of CF sputum. Reduces sputum viscoelasticity without affecting mucin or disulfide bonds.

HyperSal, MucoClear

Osmotic agent. Draws water into airway lumen → rehydrates periciliary liquid layer → restores mucociliary clearance. Also reduces sodium absorption and may reduce airway surface liquid depletion.

Survanta

Natural bovine lung surfactant extract. Contains phospholipids (primarily DPPC), neutral lipids, fatty acids, and surfactant proteins SP-B and SP-C. Reduces alveolar surface tension → prevents alveolar collapse at end-expiration.

Infasurf

Natural bovine lung surfactant extract. Contains phospholipids and surfactant proteins SP-B and SP-C. Reduces alveolar surface tension to near-zero during expiration, preventing end-expiratory alveolar collapse.

Curosurf

Natural porcine surfactant extract. Highest phospholipid concentration of available surfactants (~80 mg/mL). Contains SP-B and SP-C. Reduces surface tension at the alveolar air-liquid interface.

INOmax, Genosyl

Endogenous signaling molecule. Inhaled NO diffuses into pulmonary vascular smooth muscle → activates guanylyl cyclase → increases cGMP → vasodilation. Effect is selective to ventilated lung segments, improving V/Q matching.

Flolan, Veletri

Synthetic prostacyclin (PGI2). Binds prostacyclin receptors on pulmonary vascular smooth muscle → increases cAMP → vasodilation. Also inhibits platelet aggregation.

Revatio (PAH), Viagra (erectile dysfunction)

Phosphodiesterase-5 (PDE-5) inhibitor. PDE-5 degrades cGMP in smooth muscle. By inhibiting PDE-5 → increased cGMP → smooth muscle relaxation and vasodilation. Potentiates effect of nitric oxide in pulmonary vasculature.

Adrenalin, EpiPen, Auvi-Q

Endogenous catecholamine. Activates alpha-1 (vasoconstriction), beta-1 (increased HR and contractility), and beta-2 (bronchodilation) receptors. Dose-dependent effects: low doses primarily beta; high doses alpha-dominant.

Levophed

Endogenous catecholamine. Predominantly alpha-1 and alpha-2 agonist → peripheral vasoconstriction → increased MAP. Minimal beta-2 effects (no bronchodilation). Some beta-1 effects (inotropic) at high doses.

Intropin

Endogenous catecholamine precursor. Dose-dependent receptor activation: low doses (1–5 mcg/kg/min): dopaminergic D1 receptors → renal/mesenteric vasodilation. Moderate doses (5–10 mcg/kg/min): beta-1 → increased contractility and HR. High doses (>10 mcg/kg/min): alpha-1 → vasoconstriction.

Dobutrex

Synthetic catecholamine. Primarily beta-1 agonist (inotropic and chronotropic). Mild beta-2 effects (mild vasodilation). Negligible alpha effects — does NOT raise SVR.

Diprivan

General anesthetic/sedative. Potentiates GABA-A receptor activity → CNS depression. Mechanism not fully understood but primarily GABAergic. Provides sedation, hypnosis, and anticonvulsant properties. Has intrinsic bronchodilatory properties.

Versed

Benzodiazepine. Positive allosteric modulator of GABA-A receptors → enhances chloride influx → CNS depression. Provides anxiolysis, sedation, amnesia, and anticonvulsant effects. No analgesic properties.

Sublimaze (IV), Duragesic (patch), Actiq (lozenge)

Synthetic opioid. Binds mu-opioid receptors in CNS and periphery → analgesia via decreased pain signal transmission, altered pain perception. Also produces sedation, euphoria, respiratory depression, and GI effects.

Precedex

Selective alpha-2 adrenergic agonist. Activates central (locus coeruleus) alpha-2 receptors → decreased norepinephrine release → sedation and anxiolysis. Peripheral alpha-2 activation → decreased sympathetic outflow and pain signal transmission.

Anectine, Quelicin

Depolarizing neuromuscular blocking agent. Structurally mimics acetylcholine. Binds and persistently activates nicotinic receptors at neuromuscular junction → initial muscle fasciculations → sustained depolarization → flaccid paralysis (phase I block).

Zemuron

Non-depolarizing neuromuscular blocking agent. Competitive antagonist at nicotinic acetylcholine receptors at neuromuscular junction. Blocks ACh binding → prevents end-plate depolarization → flaccid paralysis. No fasciculations.

Norcuron

Non-depolarizing neuromuscular blocking agent. Competitive antagonist at nicotinic ACh receptors. Structurally similar to pancuronium but without vagolytic effects (no tachycardia).

Lasix

Loop diuretic. Inhibits Na+/K+/2Cl− cotransporter (NKCC2) in the thick ascending limb of Loop of Henle → blocks reabsorption of Na+, K+, and Cl− → profound diuresis. Also reduces preload via venodilation (acute effect).

Heliox

Mixture of helium (60–80%) and oxygen (20–40%). Helium is less dense than nitrogen. Lower gas density reduces turbulent flow (decreases Reynolds number) and resistance to flow in large airways. Enhances laminar flow through narrowed airways → reduces work of breathing.

Various

Divalent cation. Physiological calcium antagonist in smooth muscle → inhibits calcium-mediated bronchoconstriction → bronchodilation. Also inhibits mast cell and T-lymphocyte activation. Reduces neuromuscular transmission at high doses.

Cafcit

Methylxanthine. Competitively antagonizes adenosine receptors (A1 and A2A) in CNS → stimulates respiratory drive (chemoreceptor sensitivity to CO2). Also increases diaphragmatic contractility and reduces hypoxic depression of breathing.

Xolair

Humanized monoclonal anti-IgE antibody. Binds free IgE so it cannot attach to mast cells and basophils, and down-regulates their high-affinity IgE receptors. Blunts the allergic (type 2) cascade before it starts.

Nucala

Humanized monoclonal antibody against interleukin-5 (IL-5), the main cytokine for eosinophil growth, activation and survival. Lowers blood and airway eosinophils.

Fasenra

Humanized monoclonal antibody against the IL-5 receptor alpha on eosinophils and basophils. Triggers antibody-dependent cell-mediated cytotoxicity, so eosinophils are depleted almost completely rather than just starved of IL-5.

Dupixent

Human monoclonal antibody against the IL-4 receptor alpha subunit. Blocks signaling of both IL-4 and IL-13, reducing type 2 inflammation, IgE production, mucus hypersecretion and FeNO.

Tezspire

Human monoclonal antibody against thymic stromal lymphopoietin (TSLP), an epithelial alarmin at the top of the inflammatory cascade. Dampens both type 2 and non-type 2 airway inflammation.

Trikafta, Kaftrio (with separate ivacaftor)

Triple CFTR modulator. Elexacaftor and tezacaftor are correctors that help misfolded CFTR protein (e.g., F508del) reach the cell surface; ivacaftor is a potentiator that holds the channel open. Restores chloride and bicarbonate transport, thinning airway secretions.

Narcan, Kloxxado, Zimhi

Competitive opioid receptor antagonist (mu > kappa, delta). Displaces opioids and reverses respiratory depression, sedation and miosis.

Romazicon

Competitive antagonist at the benzodiazepine site of the GABA-A receptor. Reverses benzodiazepine sedation; less reliable for respiratory depression.

Bridion

Modified gamma-cyclodextrin that encapsulates rocuronium (and, less tightly, vecuronium) in plasma, pulling the drug off the neuromuscular junction. Works at any depth of block, without anticholinesterase side effects.

Bloxiverz

Acetylcholinesterase inhibitor. Raises acetylcholine at the neuromuscular junction to compete with non-depolarizing blockers. Also raises acetylcholine at muscarinic sites, causing bradycardia, secretions and bronchospasm unless an anticholinergic is given with it.

S2, Asthmanefrin

50:50 mix of D- and L-epinephrine (only the L-isomer is active). Alpha-1 vasoconstriction shrinks swollen subglottic and laryngeal mucosa; beta-2 effects add mild bronchodilation.

Ketalar

NMDA receptor antagonist producing dissociative anesthesia and analgesia. Releases catecholamines (raises HR and BP), preserves airway reflexes and respiratory drive at usual doses, and relaxes bronchial smooth muscle.

Amidate

Imidazole hypnotic that enhances GABA-A receptor activity. Produces rapid unconsciousness with minimal effect on blood pressure, heart rate or contractility. No analgesic effect.

Cyklokapron, Lysteda

Synthetic lysine analogue that blocks lysine-binding sites on plasminogen, preventing fibrin breakdown (antifibrinolytic).

Heparin sodium

Binds antithrombin and greatly accelerates its inactivation of thrombin (IIa) and factor Xa. Short half-life and fully reversible with protamine.

Lovenox

Low-molecular-weight heparin. Binds antithrombin and inhibits mainly factor Xa, with less anti-thrombin effect. Predictable dosing without routine monitoring.

Chantix (generic varenicline), Champix

Partial agonist at alpha-4 beta-2 nicotinic receptors. Gives enough dopamine release to ease craving and withdrawal, while blocking nicotine from smoking so cigarettes are less rewarding.

NicoDerm CQ (patch), Nicorette (gum, lozenge), Nicotrol (inhaler, nasal spray)

Delivers nicotine without the tar and carbon monoxide of smoke, relieving withdrawal and craving while the patient breaks the smoking habit.