Drugs

Question 1

Microtubule inhibitors

Answer 1

Vinca alkaloids: Inhibit polymerization
Taxanes: Inhibit depolymerization

Question 2

Drugs on Voltage-Gated-Sodium-Channels

Answer 2

Target for local anesthesia, epilepsy, chronic pain & cardiac arrythmia

Lidocaine: Voltage/Frequency dependent → Shorter AP duration → Blocks NaV in open & inactive states → Blocks pore from inside
Felcainide: Decreases conducitivity, blocks NaV1.5 in heart

Question 3

Drugs on Voltage-Gated-Calcium-Channels

Answer 3

PAA & Verapamil: Direct blockage of the pore → Slower AP
DHP: Against high blood pressure → Binds the outside in the inactive state → Stabalizes the inactive state = Allosteric modulator

Question 4

Drugs on Voltage-Gated-Potassium-Channels

Answer 4

KV11.1 (hERG) is a drug target of class III antiarrhythmics

Question 5

Drugs/Toxins Acting on Vesicular Release

Answer 5

Tetanus toxin: Splits synaptobrevin → Inhibits fusion of VGAT → Muscle cramps (no more inhibition)
Botulinum toxin: Prevents muscle contraction → Prevents excitatory vesicle fusion

Question 6

Drugs Acting on Neurotransmitter Reuptake

Answer 6

ACh Esterase Inhibitors: Curare → No cleavage of ACh
Antidepressants (SSRIs, SNRIs, TCAs) -> Suppress serotonin & NA transporters
Psychostimulants Cocaine, amphetamine, mthylphenidate: Inhibit/Reverse dopamine/NA transporters
Phencydidine & Ketamine: Dopamine transporters inhibited
Tigabine: Anticonvulsant → Inhibits GABA1 → Epilepsy treatment

Question 7

Drugs targeting AMPAR

Answer 7

Blocked by CNQX
Perampanel & Topiramate → Antiepileptics → Non-competitive antagonists that bind pocket in closed state → Harden opening

Question 8

Drugs on NMDAR

Answer 8

Blocked by APV
Valproate: Influences Na+, Ca2+ channels, NMDAR & GABA receptors
Felbamate: Modulates NMDAR

Question 9

Drugs targeting GABA-A

Answer 9

Diazepam (Benzodiazepine): Increased GABA-mediated chloride flux → Allosteric modulator → Extra binding site → Makes activation easier → Increased flow-through
Picrotoxin (Also on GlyR): Blocks the pore → Non-competitive antagonist (Stimulating)

Question 10

Drugs targetin nAChR

Answer 10

Depolarization blocking agents → Block directly AChR (Constantly open the channel)→ No depolarization & contraction (e.g. Suxamethonium)
Non-depolarization blocking agents → No more ACh binding

Question 11

Drugs acting on dopamine receptors

Answer 11

L-DOPA: Treatment of Parkinsons Disease (Precursor that can pass the BBB)
Pramipexole: Agonist of DR3 → Binds two serines normally involved in dopamine binding

Question 12

Drugs acting on GABA-B receptor

Answer 12

Baclofen: Competitive agonist for the GABA binding site → Treatment of muscle spasticity and off-label for epilepsy, alcoholic diseases….