This document provides information on the mechanisms of action of various drugs. It explains that mechanisms of action describe how drugs produce their effects in the body, such as by affecting specific targets like enzymes or cell functions. Some key points include: - Statins work by inhibiting the HMG-CoA reductase enzyme to reduce cholesterol production. - Beta-blockers inhibit beta-adrenergic receptors, mainly beta-1 receptors in the heart, to reduce heart rate and workload. - NSAIDs inhibit the COX enzyme to reduce inflammation and pain. - Opioids interact with opioid receptors to mimic endogenous opioid peptides and provide pain relief. - SSRIs inhibit serotonin reuptake to increase

1. MECHANISMS
OF ACTION!
LEARN PHARMACOLOGY
Md. Mirajul Islam, Rph
Email: mislam.samrat@gmail.com

2. WHAT ARE “MECHANISMS OF ACTION”?
 In medicine, a term used to describe how a drug or other substance produces
an effect in the body.
 For example, a drug’s mechanism of action could be how it affects a specific
target in a cell, such as an enzyme, or a cell function, such as cell growth.
Knowing the mechanism of action of a drug may help provide information
about the safety of the drug and how it affects the body. It may also help
identify the right dose of a drug and which patients are most likely to respond
to treatment. Also called MOA.

3. STATINS
ATORVASTATIN
PRAVASTATIN
Statins work by
inhibiting the HMG-
CoA reductase
enzyme; the rate-
limiting enzyme in the
mevalonate pathway
of cholesterol
production.

4. BETA-BLOCKERS
METOPROLOL - BISOPROLOL - PINDOLOL
 Beta blockers are a group of drugs that inhibit the sympathetic activation of β-adrenergic receptors. Beta-1
adrenoceptors are found on the heart. Beta-2 adrenoceptors are found on the lungs.
 Memory tool: beta-1, 1 heart; beta-2, 2 lungs! Some beta-blockers are selective for the heart and work to
reduce the force of contraction and speed of conduction of the heart. This relieves the heart from work and
oxygen demand. Beta-blockers also prolong the refractory period of the AV node, making these drugs
effective in the treatment of cardiac arrhythmias.
 Cardioselective blockers (e.g., atenolol, bisoprolol) primarily block β1 receptors in the heart, causing
decreased heart rate, cardiac contractility, cardiac workload, and AVN conduction. Nonselective beta
blockers (e.g., pindolol, propranolol) inhibit all β receptors and may cause bronchoconstriction,
peripheral vasoconstriction, and metabolic imbalances
(e.g., hypoglycemia and hyperglycemia, hypertriglyceridemia) in addition to cardiac effects.
 Cardioselective beta blockers have a lower side-effect profile and are preferred in the management
of coronary heart disease, compensated heart failure, acute coronary syndrome, and certain types
of arrhythmias.
 Propranolol, a nonselective beta blocker, is the first-line drug in the management of essential tremor, portal
hypertension, migraine prophylaxis, and thyroid storm.

5. BETA-2 AGONISTS
ALBUTEROL - SALMETEROL
 Beta-2 agonists are used in the treatment of asthma and COPD. By
stimulating (or “agonizing”) the beta-2 receptor, which is found in
the lungs, beta-2 agonists work to cause smooth muscle relaxation
– making it easier to improve air flow in the lungs.

6. CORTICOSTEROIDS
DEXAMETHASONE PREDNISOLONE
 Corticosteroids are a class of steroid hormones released by the
adrenal cortex, which includes glucocorticoids and
mineralocorticoids.
 Corticosteroids bind to surface cell glucocorticoid receptors, which
then navigate their way into the cell nucleus to alter gene
expression. Corticosteroids enhance anti-inflammatory genes and
downregulate pro-inflammatory genes.

7. TETRACYCLINES
MINOCYCLINE DOXYCYCLINE
 Proteins are necessary for cells, including bacterial cells, to survive.
Tetracyclines work by inhibiting protein synthesis inside bacterial
cells.
 Once tetracyclines have been transported into the cell, this class of
antibiotic reversibly binds to receptors on the 30S ribosomal
subunit of the bacteria, preventing attachment of aminoacyl-tRNA
to the RNA-ribosome complex. This prevents the addition of
amino acids to the elongating peptide chain, preventing synthesis
of proteins.

8. ACE INHIBITORS
CAPTOPRIL LISINOPRIL RAMIPRIL
 ACE inhibitors block the angiotensin-converting enzyme – which
normally converts angiotensin I into angiotensin II.
 Angiotensin II is responsible for effects such as vasoconstriction
(which constricts blood vessels and increases blood pressure) and
releasing the hormone, aldosterone, which works to increase blood
pressure further.
 ACE inhibitors prevent these actions from angiotensin II and
therefore they are used as antihypertensive drugs.

9. NSAIDS
NAPROXEN IBUPROFEN ETORICOXIB
 NSAIDs are non-steroidal anti-inflammatory drugs. They work by
inhibiting the cyclooxygenase enzyme, or COX.
 There are 2 kinds of COX: COX-1 and COX-2. The therapeutic
effects of NSAIDs come from COX-2 inhibition – reducing
inflammation. Therefore, NSAIDs are used to treat mild-to-
moderate pain and pain related to inflammation. Aspirin also
works by inhibiting COX.

10. OPIOIDS
CODEINE DIHYDROCODEINE TRAMADOL MORPHINE
 Opioids are used in the treatment of pain. Opioids mimic the
actions of endogenous opioid peptides by interacting with
delta or kappa opioid receptors. The opioid receptors are
coupled to G1 proteins and the actions of the opioids are mainly
inhibitory.

11. ANTIFUNGAL DRUGS
KETOCONAZOLE NYSTATIN CLOTRIMAZOLE
 Azole antifungal drugs work by targeting ergosterol in fungal cell
membranes. By targeting ergosterol, it impairs cell membrane
synthesis, cell growth, and replication – damaging fungal cells.

12. PENICILLINS
BENZYLPENICILLIN FLUCLOXACILLIN AMPICILLIN AMOXICILLIN
 Penicillins work by inhibiting enzymes responsible for linking up
key elements in bacterial cell walls. By weakening bacterial cell
walls, penicillins cause these cells to swell up, break, and ultimately
die. The antimicrobial activity of penicillins comes from the fact
that they contain a beta-lactam ring; a 4-sided square ring in their
chemical structure. Another drug class – called cephalosporins –
also contain a beta-lactam ring and work in much the same way.
Examples include cefazolin, ceftriaxone, cefdinir, and cefoperazone.

13. PROTON-PUMP INHIBITORS
LANSOPRAZOLE OMEPRAZOLE PANTOPRAZOLE
 PPIs are used to treat conditions that arise from excess gastric acid
production. PPIs work to inhibit gastric acid production by blocking
the “proton-pump” that feeds hydrogen ions into the stomach.
PPIs irreversibly bind to the H+/K+-ATPase (aka. the proton pump)
in gastric parietal cells.

14. FLUOROQUINOLONES
CIPROFLOXACIN MOXIFLOXACIN
 Fluoroquinolones are antibacterial drugs that work by inhibiting
DNA synthesis. As cells cannot replicate, the rate of production is
reduced, and this allows the body to fight off the infection.

15. BENZODIAZEPINES
DIAZEPAM MIDAZOLAM NITRAZEPAM
 Benzodiazepines are used to treat anxiety, seizures, to induce
anesthesia, and insomnia. They work by enhancing the binding of
the neurotransmitter GABA to the GABA A receptor. Once bound, it
causes a “depressive” effect on neuronal synaptic transmission that
lead to reduced anxiety, sleepiness, sedation, and an anticonvulsive
effect.

16. ANTIPSYCHOTICS
HALOPERIDOL CHLORPROMAZINE RISPERIDONE CLOZAPINE
 Antipsychotics work by a complex range of methods, but one of
the most common is blocking post-synaptic D2 receptors. D2
receptors are “dopaminergic” receptors that impact dopamine
levels. D2 blockade is one of the primary ways that antipsychotic
drugs reduce psychotic symptoms in affected patients.

17. SSRIS
FLUOXETINE PAROXETINE SERTRALINE
 SSRIs are “selective serotonin reuptake inhibitors”. Whereas
antipsychotics act on dopamine receptors, SSRIs act on serotonin
levels. Specifically, SSRIs work to inhibit neuronal reuptake into
neuronal cells. This means more serotonin is available between
neurons to increase neurotransmission.

18. ANTIHISTAMINES
CETIRIZINE LORATADINE FEXOFENADINE CHLORPHENIRAMINE
 These 4 drugs are antagonists of the histamine, H1 type. H1
antagonism prevents the release of histamine from granules found
in mast cells. Histamine is responsible for pro-allergy effects.
Hence, these drugs are used to treat allergies, hay fever, itch, and
hives.

19. ANTIHISTAMINES
RANITIDINE
 Ranitidine is a histamine H2 antagonist used to treat duodenal ulcers,
Zollinger-Ellison syndrome, gastric ulcers, GERD, and erosive esophagitis.
 After a meal, the hormone gastrin, produced by cells in the lining of the
stomach, stimulates the release of histamine, which then binds to histamine
H2 receptors, leading to the secretion of gastric acid. Ranitidine reduces the
secretion of gastric acid by reversible binding to histamine (H2) receptors,
which are found on gastric parietal cells. This process leads to the inhibition
histamine binding to this receptor, causing the reduction of gastric acid
secretion. The relief of gastric-acid related symptoms can occur as soon as
minutes after administration of a single dose, and the effects can last from
10 hours, providing fast and effective symptomatic relief.

20. HEPARIN
 Heparin is an anticoagulant indicated for thromboprophylaxis
and to treat thrombosis associated with a variety of conditions
such as pulmonary embolism and atrial fibrillation.
 To make clots, you need thrombin and factor Xa; two key
in the clot forming pathway. Heparin works to inactivate factor Xa
and thrombin. There are low-molecular weight versions of
too, and these drugs preferentially inhibitor factor Xa. Examples
include enoxaparin and dalteparin.

21. WARFARIN
 Warfarin is a vitamin K antagonist used to treat venous
thromboembolism, pulmonary embolism, thromboembolism with
atrial fibrillation, thromboembolism with cardiac valve
and thromboembolic events post myocardial infarction
 Warfarin is a [vitamin K] antagonist which acts to inhibit the
production of vitamin K by vitamin K epoxide reductase. The
reduced form of vitamin K, vitamin KH2 is a cofactor used in the
carboxylation of coagulation factors VII, IX, X, and thrombin.

22. METFORMIN
 The glucose-lowering, insulin-sensitizing agent metformin works mainly by reducing gluconeogenesis and
opposing glucagon-mediated signalling in the liver and, to a lesser extent, by increasing glucose uptake in
skeletal muscle
 The primary site of metformin action is the mitochondrion
 The antihyperglycaemic effect of metformin is probably owing to defective protein kinase A signalling
 Metformin affects lipid metabolism primarily via 5′-AMP-activated protein kinase (AMPK) activation
 Antitumourigenic effects of metformin, which require further study, might be partially due to systemic
metabolic alterations, including the reduced availability of insulin
 In cancer cells, metformin acts as an inducer of energetic stress; AMPK-driven inhibition of mTOR seems to be
required for much of its antimitotic activity
 Metformin is used in the treatment of type 2 diabetes. It works by increasing the sensitivity (or “response”) to
insulin. For example, this means it suppresses glucose production by the liver, increases glucose uptake into
skeletal muscle, and it suppresses glucose absorption by the intestines. This collectively works to reduce blood
sugar levels.