Grouped by how the drug actually works — what it does at the receptor, enzyme, channel or pump. This one cuts across body systems on purpose: a beta blocker and an antipsychotic are both receptor blockers, and seeing that is the point. Same 959 drugs.
HA high-alert drug · BBW has a black box warning · click any drug to open its card.
Sit on adrenaline's receptors so the sympathetic signal cannot land. Beta-1 blockade in the heart slows rate and force; alpha-1 blockade relaxes vessel walls, the bladder neck and the prostate.
-olol takes the foot off the heart's gas pedal; -osin loosens the pipes, blood and urinary.
The hormones are still made, but their receptors are plugged. Blocking AT1 keeps vessels dilated; blocking the aldosterone receptor in the distal nephron dumps sodium and water while holding potassium back.
-sartan locks angiotensin out of the door; spironolactone locks aldosterone out and keeps the K+.
Block acetylcholine at muscarinic receptors, so the parasympathetic 'rest and digest' signal is cut off. Secretions dry up, heart rate rises, gut and bladder muscle relax, and pupils dilate.
Can't see, can't pee, can't spit, can't poop - and hot as a hare.
Occupy histamine's receptor so histamine cannot trigger it. H1 blockade in skin and vessels stops itch, hives and swelling; H2 blockade on the stomach's parietal cell turns acid production down.
H1 is skin and nose, H2 is stomach - and first-generation H1 drugs cross into the brain and knock you out.
Block dopamine D2 receptors in the brain's limbic pathway, turning down the dopamine overactivity behind hallucinations and delusions. Second-generation agents also block 5-HT2A, which softens the motor side effects.
Block dopamine everywhere it goes: mood improves, movement suffers, prolactin rises.
Block the receptors for the body's own signalling molecules - CGRP, leukotrienes, endothelin, vasopressin. The mediator is still released; it simply has nowhere to land.
-gepant blocks migraine's CGRP, -lukast locks out leukotrienes, -sentan opens the lung, -vaptan wastes water.
Plug a CNS receptor that drives one specific unwanted signal: 5-HT3 on the vagus and vomiting center, NK1 for delayed vomiting, orexin for wakefulness, NMDA and AMPA for runaway excitation.
-setron cuts the vomit wire; -pitant kills the second-day nausea; -orexant switches the wake signal off.
Cut the sex-hormone signal in one of two places. Receptor blockers sit on the estrogen or androgen receptor so the hormone cannot switch growth genes on; GnRH agents work upstream at the pituitary so the gonads are never told to make the hormone at all.
Block the seat, or cut the phone line to the factory.
Act at the nicotinic receptor of the neuromuscular junction. Nondepolarizers plug the receptor so acetylcholine cannot act; succinylcholine over-activates it and leaves the membrane stuck depolarized.
Paralysis only - the patient feels and hears everything unless you sedate them.
Compete with opioids at the mu receptor and win, knocking the opioid off. Central antagonists reverse sedation and respiratory depression; peripheral ones only free up the gut.
Naloxone kicks the opioid off the receptor - fast, and the patient wakes up angry.
Switch on beta-2 receptors on bronchial smooth muscle, which relaxes the airway and widens it within minutes. The same receptors in skeletal muscle and the heart explain the shakes and the racing pulse.
-terol: opens the tubes and revs the motor.
Directly stimulate alpha and beta receptors the way the body's own adrenaline does. Alpha-1 squeezes vessels and raises pressure; beta-1 raises heart rate and force; beta-2 opens airways.
Fight-or-flight in a syringe - the receptor MIX decides the effect. Not all of them are catecholamines: phenylephrine and midodrine are not.
Stimulate alpha-2 receptors in the brainstem, which act as a brake on sympathetic outflow. Less norepinephrine leaves the CNS, so heart rate, vessel tone and blood pressure all fall.
An adrenergic drug that CALMS - alpha-2 is the off switch, not the on switch.
Restore dopamine signalling in the striatum. Agonists stimulate the dopamine receptor directly, bypassing the dying neurons; levodopa instead supplies the raw material the surviving neurons convert into dopamine.
Levodopa refills the tank; the -ole agonists skip the tank and press the pedal.
Bind mu opioid receptors in the spinal cord and brain, closing the gate on pain signals and changing how pain feels. The same receptors in the brainstem and gut slow breathing and slow the bowel.
Mu = miosis, morphine, muted breathing, motionless gut.
Stimulate 5-HT1B receptors on dilated meningeal vessels so they constrict, and 5-HT1D receptors on trigeminal nerve endings so they stop releasing inflammatory peptides.
-triptan: tightens the throbbing vessel and quiets the nerve.
Sit at a side pocket of the GABA-A chloride channel and make the brain's own GABA far more effective. Chloride pours in, the neuron is harder to fire, and the whole CNS is turned down.
Does not open the door itself - it holds the door open longer for GABA.
Two ways to work the same gut hormone: the -tides stimulate the GLP-1 receptor directly, while the -gliptins block DPP-4, the enzyme that chews GLP-1 up, so the body's own hormone lasts longer. Either way insulin is released only when glucose is high and glucagon is suppressed.
-glutide pushes the button, -gliptin stops the body from taking the finger off it.
Supply or mimic prostaglandins at their own receptors. Depending on the receptor they open the eye's uveoscleral drain, dilate pulmonary arteries, protect gastric mucosa, or ripen the cervix and contract the uterus.
-prost-: prostaglandin in the name, and it always relaxes or opens something.
Deliver nitric oxide - or act like it - inside vascular smooth muscle, raising cyclic GMP so the vessel wall relaxes. Veins dilate first, which drops preload and the heart's oxygen demand; arteries follow at higher doses.
Nitric oxide is the body's own 'relax' molecule; nitrates hand it over directly.
A mixed set that all work by switching a specific receptor ON - acetylcholine, vasopressin, thrombopoietin, calcium-sensing, melatonin, GABA-B, PPAR-alpha, 5-HT4, guanylate cyclase-C, beta-3 and sphingosine-1-phosphate.
Different receptors, same trick - press the button the body normally presses.
Block the enzyme that converts angiotensin I into angiotensin II, so the body simply cannot make its strongest vasoconstrictor. The same enzyme normally destroys bradykinin, which now builds up.
-pril: no angiotensin II means no squeeze - and the leftover bradykinin gives the dry cough.
Block HMG-CoA reductase, the rate-limiting enzyme of cholesterol production in the liver. The liver, short on cholesterol, pulls more LDL out of the blood by making extra LDL receptors.
-statin: shuts down the liver's cholesterol factory line.
Block cyclooxygenase, the enzyme that turns arachidonic acid into prostaglandins. Less prostaglandin means less pain, fever and inflammation - but also less protection for the stomach lining and less blood flow to the kidney.
No prostaglandin, no pain - and no stomach lining either.
Block the enzyme that destroys cyclic AMP and cyclic GMP, so those second messengers pile up inside the cell. Smooth muscle relaxes, the heart contracts harder, and inflammatory cells quiet down - which one happens depends on the PDE subtype.
Stops the cleanup crew, so the 'relax' signal keeps shouting.
Block the enzymes that break a neurotransmitter down, so more of it stays in the synapse. Cholinesterase inhibitors preserve acetylcholine; MAO-B and COMT inhibitors preserve dopamine.
Do not make more - just stop the shredder.
Sit in the ATP pocket of a signalling kinase - the enzyme a cancer or immune cell uses to relay 'grow and divide' or 'inflame'. With the relay switch jammed the growth or inflammation signal never reaches the nucleus.
-nib: it NIBbles the growth signal. -citinib: JAK is the inflammation relay.
Disable a step the virus cannot skip: the protease that cuts new proteins to size, the integrase that staples viral DNA into ours, the polymerase and neuraminidase that copy and release new virions, or the envelope proteins it uses to get in at all.
-navir cuts nothing, -gravir staples nothing, -tamivir escapes nothing.
Stop HIV's reverse transcriptase from copying viral RNA into DNA. Nucleoside analogs get built into the growing chain and end it; non-nucleosides bend the enzyme out of shape.
Reverse transcriptase is the virus's photocopier - the NRTI is a jammed sheet of paper.
Attack enzymes bacteria need to handle their own genetic material - DNA gyrase and topoisomerase IV for the quinolones, DNA-dependent RNA polymerase for the rifamycins. The bacterial chromosome cannot be unwound or transcribed.
-floxacin unwinds nothing; rif- turns everything orange.
Block the enzyme that MAKES a substance rather than the receptor it acts on - the aromatase that builds estrogen, the 5-alpha-reductase that builds DHT, xanthine oxidase that builds uric acid, carbonic anhydrase, lipase, and the gut enzymes that release glucose.
Do not block the hormone - shut down the factory that makes it.
Block the machinery a cancer cell uses to survive its own damage: PARP that patches broken DNA, the proteasome that clears worn-out proteins, and the histone enzymes and export proteins that control which genes get read.
The cell can still break - it just cannot fix or tidy up afterwards.
Plug the L-type calcium channel so calcium cannot enter the cell. In vessel walls that means relaxation and lower pressure; in the heart's conduction tissue it means a slower rate and weaker contraction.
-dipine relaxes the PIPES; verapamil and diltiazem slow the PUMP.
Change the shape of the cardiac action potential by blocking a specific channel. Sodium blockers slow how fast the impulse travels; potassium blockers lengthen repolarization so the cell cannot refire too soon.
Sodium slows the upstroke; potassium stretches the reset - and stretching the reset stretches the QT.
Hold voltage-gated sodium channels in their inactive state, so a neuron that is already firing too fast cannot keep firing. Normal traffic gets through; a seizure's runaway train does not.
Use-dependent: the busier the neuron, the harder the drug clamps it.
Shut the ATP-sensitive potassium channel on the pancreatic beta cell. The cell depolarizes, calcium rushes in, and stored insulin is squeezed out whether or not glucose is actually high.
Close the K+ door, force the insulin out - glucose has no say in it.
Everything else that works by changing what an ion channel does: calcium channel subunit binders in nerve terminals, epithelial sodium channel blockers in the nephron, chloride channel openers in the gut, and the funny-current and late-sodium channels in the heart.
Find the channel, find the effect - the ion that moves tells you the side effect.
Bind the H+/K+ ATPase - the final pump that physically pushes acid into the stomach - and disable it permanently. That pump is done; acid output only returns as new pumps are built.
-prazole: not turning acid down, unplugging the pump entirely.
Block the transporter that vacuums serotonin or norepinephrine back into the presynaptic neuron. The neurotransmitter stays in the synapse longer, and over weeks the receptors adapt - which is why the mood effect is delayed.
The vacuum cleaner is unplugged, so the serotonin stays on the floor.
Block - and in the amphetamines, reverse - the dopamine and norepinephrine transporters, so those transmitters flood the synapse. Alertness, focus, heart rate and blood pressure all rise together.
Same transporter trick as an antidepressant, but on dopamine - so it works in an hour, not a month.
Block the sodium-glucose cotransporter in the proximal tubule, so glucose that was filtered is not reabsorbed. Sugar leaves in the urine, taking water and sodium with it.
-gliflozin: makes the kidney pee out the sugar.
Block a specific sodium transporter in the nephron so that sodium - and the water that follows it - is not reabsorbed. Loops hit the Na-K-2Cl carrier in the thick ascending limb; thiazides hit the Na-Cl carrier in the distal tubule.
Loops blast (the powerful one), thiazides trickle - and both wash potassium out the door.
Block a specific carrier so a substance cannot be moved where it usually goes: the sodium-potassium pump in the heart, urate and bile-acid carriers in kidney and gut, cholesterol uptake in the intestine, and the vesicle transporter that loads dopamine.
Every one of these stops a shuttle bus - find the cargo and you have the effect.
Block a single clotting factor in the middle of the cascade. The -xabans sit on factor Xa; the -atrans and -rudins block thrombin itself; the heparins work indirectly by supercharging antithrombin.
-Xa-ban tells you the target out loud: BAN factor Xa. The -xabans, -atrans and -rudins hit the factor DIRECTLY; the heparins do it INDIRECTLY, through antithrombin.
Block the enzyme that recycles vitamin K, so the liver cannot finish building factors II, VII, IX and X. Existing factors keep working until they expire, which is why the effect takes days.
1972 - factors 10, 9, 7, 2 are the ones that need vitamin K.
Stop platelets sticking to each other. The -grels block the ADP (P2Y12) receptor that activates the platelet; the IIb/IIIa blockers cover the final receptor that fibrinogen uses to bridge platelets together.
ADP blockers stop the invitation; IIb/IIIa blockers cut the handshake itself.
Convert plasminogen into plasmin, the enzyme that digests fibrin. Unlike every anticoagulant, these dissolve a clot that already exists.
-plase: it PLAYS the clot apart. Anticoagulants prevent; only these destroy.
The beta-lactam ring binds the penicillin-binding proteins that cross-link peptidoglycan. Without cross-links the wall cannot be finished, and internal pressure bursts the bacterium.
The wall gets built with no mortar - the cell pops.
Bind the building block of the wall itself rather than the enzyme, so the bricks can never be laid. Daptomycin goes further and punches holes in the membrane, letting potassium leak out.
Not blocking the bricklayer - grabbing the brick.
Fungal membranes use ergosterol where ours use cholesterol. Azoles and allylamines block the enzymes that build ergosterol, polyenes bind it and tear pores in the membrane, and echinocandins block the glucan wall instead.
Ergosterol is the fungus's cholesterol - break it and the membrane leaks.
Attack a structure or pathway only the organism has. TB drugs block the waxy mycolic acid wall or the organism's ATP supply; antimalarials poison the parasite's ability to detoxify heme; topical scabicides paralyze the arthropod's own nerve channels.
RIPE for TB - Rifampin, Isoniazid, Pyrazinamide, Ethambutol; and the antimalarials poison what the parasite eats.
Stick a reactive chemical group onto DNA, cross-linking the two strands so they cannot separate. The cell cannot copy or read its own genome and dies - the nitroimidazoles do the same thing to anaerobes using free radicals.
Superglue for DNA: the strands can never unzip again.
Counterfeit building blocks. They look enough like a real nucleotide - or like folate, which is needed to build nucleotides - that the cell picks them up, and then the DNA or RNA chain jams. The same trick that starves a tumor also stops a virus copying itself.
A fake brick in the wall: the builder keeps laying, and the wall collapses.
Wedge between DNA base pairs and freeze the enzymes that unwind and re-seal the double helix. The strand is cut and never repaired, and free radicals from the drug add more breaks.
The zipper is opened and the drug jams it - the DNA can never close again.
Attack the microtubule, the rope the cell uses to pull chromosomes apart. Vincas stop the rope from forming; taxanes freeze it so it can never let go. Either way mitosis stalls and the cell dies.
Vinca = no rope. Taxane = rope stuck. Mitosis stops either way.
Lock onto the small 30S subunit of the bacterial ribosome. Aminoglycosides make it misread the code and build nonsense protein; tetracyclines block the incoming tRNA so the chain never grows.
Bacteria have 30S and 50S; we have 40S and 60S - that is the whole reason these are safe for us.
Bind the large 50S subunit and stop the growing protein chain from moving along the ribosome. Protein production halts, so the bacterium cannot grow or repair itself.
Macrolides, clindamycin and linezolid all crowd the same 50S seat - which is why they compete with each other.
Work on the message rather than the protein. Antisense strands and siRNA bind a specific mRNA so it is destroyed or read differently; gene therapies insert a working copy of the gene into the patient's own stem cells.
Fix the recipe, not the meal.
Slip into the cell, bind a receptor in the cytoplasm, and travel to the nucleus to change which genes are transcribed. Inflammatory proteins are switched off and anti-inflammatory ones switched on - which is why the effect takes hours, not minutes.
Not a fast-acting drug - it rewrites the cell's instructions.
Cripple the T lymphocyte itself. Calcineurin inhibitors block the signal that makes IL-2, so T cells never get the order to multiply; the antiproliferatives block the purine supply lymphocytes uniquely depend on.
No IL-2 signal, no T cell army.
Antibodies and fusion proteins that grab a specific inflammatory messenger - TNF-alpha, an interleukin, or IgE - or block its receptor, so the inflammatory conversation is cut off before it starts.
Take one voice out of the immune conversation and the whole argument quiets down.
Antibodies aimed at a protein on or around a cancer cell. Some block a growth-factor receptor (HER2, EGFR) or the VEGF that builds tumor blood vessels; checkpoint antibodies instead release the brake the tumor puts on T cells.
-mab is a guided missile; checkpoint drugs take the muzzle off your own T cells.
Ready-made antibodies aimed at a target that is not a cytokine or a tumor: a bone signal, a complement protein, a clotting factor, an integrin, a toxin, or - with pooled human immune globulin - whatever the donors were immune to.
Borrowed immunity: the antibody is made outside the patient and simply handed over.
Give the body more of a signalling protein instead of blocking one. Colony-stimulating factors tell the marrow to build neutrophils or red cells; interferons switch on antiviral and antitumor defences.
The opposite of a blocker - this is the immune system's megaphone.
Supply the hormone the body is not making enough of. The drug IS the signal - it binds the same nuclear or membrane receptor the natural hormone would, so the dose has to match physiology, not a symptom.
Not blocking anything - just refilling an empty tank.
Bind tightly to the mineral surface of bone and sit there. When an osteoclast tries to chew that bone up it swallows the drug, its internal enzyme pathway fails, and the osteoclast dies - so breakdown slows and density climbs.
-dronate: poison bait laid on the bone for the cells that eat it.
Replace a cofactor or ion the body runs on. Vitamins slot into enzymes as helper molecules; electrolytes and minerals restore the gradients nerves, muscle and the heart depend on.
These are ingredients, not drugs - the body already knew what to do with them.
Physically grab a substance and take it out of circulation. Resins and binders trap it in the gut so it leaves in the stool; chelators and reversal agents latch onto it in the blood so the kidney can clear it.
Chemical handcuffs - nothing is switched on or off, something is simply removed.
Work by physics and chemistry rather than by any receptor. Osmotic agents hold water where it is drawn; surfactants and lubricants soften; coating agents form a physical barrier over damaged tissue.
No receptor, no enzyme - water, oil, a barrier, or a poke at the bowel wall.
Supply an enzyme the patient cannot make, stabilise a misfolded protein, or shift how a cell handles fuel. The target is the body's own metabolism rather than a receptor or a pathogen.
Give back the missing worker, or change what the cell burns.
These drugs either work through several mechanisms at once or through a pathway that is genuinely not settled. They are parked here on purpose - a confidently wrong mechanism is worse than an honest 'not sure'.
If you cannot name the target, do not invent one - look it up before you teach it.