PHA320 -DRUG MoAs

CLASS DRUG NAME MoAs

Cholinergic Transmission - Acetylcholine (Ach) - Mimic the effect of ACh by
(Parasympathomimetic) - Pilocarpine binding directly to
Directly Acting cholinoreceptors.
Cholinergic Agonists
Cholinergic Transmission - Neostigmine - USED:
(Parasympathomimetic) - Edrophonium.  To stimulate bladder
Indirectly Acting and GIT.
Cholinergic Agonists  Myasthenia Gravis
(Anticholinesterases)
Cholinergic Transmission - Atropine - Inhibit the muscarinic
(Parasympatholytic) - Hyoscine actions of Ach resulting in
Cholinergic Antagonists (Scopolamine) an anticholinergic response
(Muscarinic - Ipratropium (Atrovent)
Antagonists)
- Botulinum Toxin - The inhibition of ACh leads
Cholinergic Transmission to the accumulation of ACh
(Parasympatholytic) in the synaptic cleft
Inhibitors of ACh resulting in overstimulation
Release of nicotinic and muscarinic
ACh receptors and impeded
neurotransmission.
- Epinephrine - Adrenergic agonists are
Adrenergic Transmission (Adrenaline) drugs that work by
(Sympathomimetics) - Norepinephrine mimicking the functioning
Direct Acting (Noradrenaline) of the SNS, direct acting
(Adrenergic Receptors - Dopamine agonist are a drug that
Agonists) - Dobutamine directly activates receptors.
- Salbutamol
(Ventolin)
Adrenergic Transmission - Amphetamine - Indirect-acting agonist
(Sympathomimetics) - Tyramine blocks the reuptake of NE or
Indirectly Acting causes the release of NE
(Adrenergic Agonists) from the vesicles of
adrenergic neurons.
 - Ephedrine. A mixed-acting agonist is a drug
Adrenergic Transmission - Pseudoephedrine that indirectly releases NE and also
(Sympathomimetics) directly activates receptors.
Mixed Action
(Adrenergic Agonists)

- Prazosin - They bind to

adrenoreceptors but do not
trigger an intracellular
Adrenergic Transmission response.
(Sympatholytic) - It is an Alpha 1- receptor
Alpha - Adrenergic blocker.
Antagonists - It decreases peripheral
(Alpha-blockers) vascular resistance and
blood pressure by relaxation
of blood vasculature smooth
muscles.
- Propranolol - They bind to
- Timolol adrenoreceptors but do not
Adrenergic Transmission trigger an intracellular
(Sympatholytic) response.
Beta-Adrenergic - They are classified
Antagonists according to their affinity to
(Beta-Blockers) α and β receptors
(Non-selective β - Non -selective b- blockers
Antagonist) means they block both beta
1 and beta 2 receptors, so
affect the heart and lungs.
- Atenolol - block only the beta 1
- Bisoprolol receptors so mostly affect
Adrenergic Transmission - Metoprolol the heart and cause a
(Sympatholytic) reduction in CO.
Beta-Adrenergic
Antagonists
(Beta-Blockers)
(Selective β Antagonist)
 - Thiazide Diuretics - Sodium and water excretion.
- Loop Diuretics - Decrease the extracellular
- Potassium Sparing volume.
Diuretics Diuretics - Decrease COP.
- Decreased Na+ causes
vascular smooth muscles
relaxation.
- Decrease peripheral
resistance
- Carvedilol - work by decreasing the
 + The beta blockers activation of B1 in the heart
mentioned above which decreases the cardiac
output and then decreases
β Blockers BP. It also decreases the
renin which leads to a
decrease in the angiotensin
II and decreases the
peripheral resistance ending
up with a decrease in BP.
- Enalapril. - ACE inhibitors lower blood
- Lisinopril. pressure by preventing the
- Perindopril. production of angiotensin II,
so decreased angiotensin II
Angiotensin-converting will lead to decreased
enzyme inhibitors aldosterone production and
(ACEI) then decrease the output of
SNS and decrease the
retention of sodium and
water. It also will increase
the level of bradykinin and
increases the vasodilation of
vascular smooth muscle
which ends up with a
decrease in BP
- Losartan. - Similar effect to ACEI but
Angiotensin II Receptor - Valsartan. no effect on bradykinin
Blockers (ARBs)
 - Nifedipine. - CCB blocks Ca++ channels
Calcium Channel - Amlodipine. in the heart and vascular SM
Blockers - Diltiazem. so inhibiting inward
(CCB) - Verapamil. movement of Ca++.

- Methyldopa - Converted to alpha-methyl

norepinephrine, a potent
Centrally Acting selective alpha-2 adrenergic
Antihypertensives agonist. Also, the
Stimulation of alpha 2
receptors in the brain result
in a fall in blood pressure.
- Nitrates - Vasodilators decrease
preload & afterload.
- Dilation of venous blood
vessels leading to increased
Vasodilators venous capacitance.
- Arterial dilation leading to
decreased systemic
arteriolar resistance.
- Nitrates are venous
vasodilators to decrease
preload in HF.
- Digitalis (Cardiac - Digoxin stops calcium from
glycosides). exiting the myocardial cell
- Digoxin causing:
- Digitoxin (Withdrawn)  Increased force of
myocardial contraction.
 Increased CO & renal
Inotropic Agents perfusion (increasing
urine output, decreasing
blood volume, and
decreasing renin
release).
 Decreased conduction
velocity through the AV
node (therefore slowing
of the heart rate).
- Dobutamine - Selectively increases cardiac
contractility (positive
β - Adrenergic Agonists inotropic effect) through
activation of β1 receptors in
the heart.
 - Acetyl Salicylic acid - Aspirin irreversibly blocks
(Aspirin). TXA2 synthesis from
Platelet Aggregation - Clopidogrel (Plavix). arachidonic acid in platelets
Inhibitors - Dipyridamole by inhibition of COX
enzyme.
- Clopidogrel acts by
Inhibiting exogenous ADP-
dependent platelet
activation.
- Heparin - Act by inhibiting the action
- LMWHs: of coagulation factors.
Enoxaparin + - Antithrombin III inhibits
Dalteparin several clotting factors
including factor IIa
Anticoagulant (thrombin) and Xa, In the
(Thrombin Inhibitors) absence of heparin it
interacts very slowly, With
heparin, antithrombin
changes conformation and
rapidly inactivates
circulating thrombin (IIa)
and factor Xa.
- LMWH complex with
antithrombin III to
inactivate factor Xa but not
thrombin (IIa).
- Warfarin - Act by interfering with the
Anticoagulants synthesis of coagulation
(Vitamin K Antagonists) factors.
- Liver uses Vit. K to
synthesize factors II, VII,
IX, X. Warfarin interferes
with the use of Vitamin K in
the synthesis of these
clotting factors, this leads to
a reduction in the activity of
circulating factors and
therefore an anticoagulant
effect.
 - Streptokinase - Used in acute
- Alteplase thromboembolic disease in
selected patients, they
degrade fibrin and dissolve
the clot.
Thrombolytic Drugs - Fibrin polymerizes and
constitutes a “mesh” that
acts as hemostatic clot (in
conjunction with platelets)
over a wounded site,
Thrombolytics catalyzes
conversion of plasminogen
to plasmin which results in
clot lysis.
- Simvastatin - Inhibition of HMG CoA
- Atorvastatin Reductase Enzyme.
- Fluvastatin - Increase in LDL Receptors:
1. Depletion of
intracellular
cholesterol in
HMG CoA Reductase hepatocytes.
Inhibitors (Statins) 2. Increased synthesis
of surface LDL
receptors to
internalize LDL.
3. Decrease plasma
cholesterol.
4. Decreased
cholesterol synthesis.
5. Increased LDL
Catabolism.
- Bezafibrate. - They decrease plasma TG
- Gemfibrozil. by increasing expression of
LPL enzyme that hydrolyzes
Fibrates TG in chylomicrons and
VLDL •
- They can also increase HDL
levels and decrease
cholesterol levels by
increasing its biliary
excretion.
 - Aspirin - Irreversible inhibition of
COX enzyme causing
Non-Steroidal Anti- inhibition of PG synthesis
Inflammatory Drugs
(NSAIDs)

- Indomethacin - Indomethacin USED TO

- Diclolfenac (Voltaren) TREAT:
Acetic Acid Derivatives 1. Osteoarthritis.
(NSAIDs) 2. Gout.
3. Patent Ductus
Arteriosus.
- Diclolfenac One of the most
potent agents
- Ibuprofen - Ibuprofens have least GI SE
Propionic Acid
Derivatives
(NSAIDs)

- Mefenamic Acid - Diarrhea may be more

severe and associated with
Fenamates bowel inflammation.
(NSAIDs)

- Celecoxib - Selective COX-2 inhibitors

are thought to act only at
Selective COX-2 sites of trauma and therefore
Inhibitors have a lower risk of SE.

- Paracetamol - Has both analgesic and

(Acetaminophen) antipyretic properties.
NSAIDs - Weak anti-inflammatory
properties.
- No effect on platelet
function
 - Oral agent: 1. Enter cell by passive
Prednisolone + diffusion.
Dexamethasone 2. Interact with Intracellular
Glucocorticoid Receptors:
Corticosteroids - IM route: Nuclear receptor regulating
Methylprednisolone gene transcription.
3. Believed to inhibit
synthesis of inflammatory
mediators.
4. Inhibit early and late
manifestations of
inflammation.
- Methotrexate - Mainstay of RA and
psoriatic arthritis treatment.
Disease Modifying Anti- More effective, faster onset,
Rheumatic Drugs Safer compared to other
(DMARDs) DMARDs.
- Immunosuppressant drug.
- Anti-malarial Drugs:
Chloroquine
Other DMARDs - Gold Salts.
- D-Penicillamine. ----

- Infliximab - Monoclonal antibodies.

Tumor necrosis factor - Adalimumab - TNF is overexpressed in
(TNF) inhibitors RA.
Biological Agents(MAB) - Blockade of its actions
caused a reduction in the
release of other
proinflammatory cytokines.
- Morphine - Binds to opioid receptors
- Meperidine and stimulates them
Opioid drug - Methadone
Strong Agonists - Fentanyl
- Heroin

- Codeine - Binds to opioid receptors

Opioid drug and stimulates them
Moderate Agonists
 - Pentazocine - Binds to opioid receptors
Opioid drug and stimulates them
Mixed Agonist- - Agonist on κ receptors. •
Antagonist Weak antagonist at µ and δ
receptors
- Tramadol - Binds to the µ-opioid
Other Analgesics receptor.
- Weakly inhibits reuptake of
NE and serotonin
- Naloxone - These bind with a high
Opioid drug affinity to opioid receptors
Antagonists but fail to activate the
receptor mediated response
- Binds to opioid receptors
and can reverse and block
the effects of other opioid's
such as heroin morphine
- Salbutamol (Ventolin) - Selective β2 agonists with a
Adrenergic Agonists: rapid onset (15 to 30 min)-
Short Acting (SABA) Maximum bronchodilation
through β2 stimulation with
minimum effect on β1
receptors
- Salmeterol - Long acting Selective β2
Adrenergic Agonists: - Formoterol agonists.
Long Acting (LABA)

- Beclomethasone - They decrease number and

- Budesonide activity of cells involved in
Corticosteroids - Fluticasone inflammation:
(Asthma) 1. Macrophages.
2. Eosinophils.
3. Lymphocytes.
- Cromolyn - Mast cell stabilizer (prevent
Alternative Drugs release of chemical
(Asthma) mediators upon antigen-
antibody binding to the mast
cell).
- Ipratropium (Atrovent) - Block parasympathetic ANS
Alternative Drugs leading to decrease in
Antimuscarinics airway smooth muscles
(Asthma) contraction & mucous
secretion.
 - Theophylline - Relaxation of smooth
Alternative Drugs - Aminophylline muscle of bronchioles,
Antimuscarinics leading to bronchodilation.
(Asthma)

- Montelukast - Block the lipo-oxygenase

enzyme OR leukotriene
Alternative Drugs receptors to prevent action
Anti-Leukotrienes of leukotrienes on the lungs:
(Asthma) 1. Inflammation.
2. Bronchoconstriction.
3. Mucous secretion.

- Cimetidine - Competitively block the

H2 Receptor Antagonists - Ranitidine binding of Histamine to H2
(H2 receptor blockers) receptors, Causing a
decreased secretion of
gastric acid.
- Omeprazole - Released and absorbed in
- Lansoprazole the small intestine.
- Transported to parietal cell
where it is activated.
Inhibitors of the H+ / K+ - Forms a stable covalent
ATPase Proton Pump bond with the proton pump
(PPI) to suppress acid secretion.
- PPI >> H2 receptor
blockers in suppressing acid
production and healing
ulcers.

- Misoprostol - Inhibits secretion of gastric

HCl.
- Stimulates secretion of
Mucous and Bicarbonate.

Prostaglandin Analogues
(PG)
 - Aluminum Hydroxide - Antacids (weak bases) +
+ Magnesium Gastric Acid = Salt and
Hydroxide Water (neutralization).
- Calcium Carbonate - Antacids work by
- Sodium Bicarbonate neutralizing gastric acid to
give salt and water,
Antacids therefore reducing Gastric
Acidity.
- Reducing Gastric Acidity
Would Result in:
1. Decrease peptic activity
since pepsin is inactive at
pH > 4.
2. Help in Reduction of H.
pylori colonization.

- Penicillin G - Inhibit bacterial cell wall

(Benzylpenicillin) synthesis.
- Resulting in cell lysis
- Penicillin V
(Bactericidal).
(Phenoxymethylpenicillin) - Act on proliferating
- Amoxycillin bacteria.
β-lactams - Little or no effect on
(Amoxil)
Penicillin Antibiotic bacteria not growing or not
- Cloxacillin dividing.
(Orbenin )
- Piperacillin
(Piprel)

- Cephalexin - Inhibit bacterial cell wall

β-lactams synthesis.
Cephalosporins - Gram Positive & Few Gram
Antibiotic Negative.
(1 st Generation) - Used for Community
acquired infection.
 - Cefuroxime - Inhibit bacterial cell wall
β-lactams - Cefuroxime axetil synthesis.
Cephalosporins - Less Gram Positive & more
Antibiotic Gram Negative than 1 st
(2 nd Generation) Gen.
- Used for Severe Community
acquired infection.
- Ceftriaxone - Inhibit bacterial cell wall
β-lactams - Ceftazidime synthesis.
Cephalosporins - Broad spectrum activity
Antibiotic against some Gram Positive
(3 rd Generation) & expanded Gram Negative.
- Used for Community
acquired infection.
- Cefepime - Inhibit bacterial cell wall
β-lactams synthesis.
Cephalosporins - Broad spectrum activity
Antibiotic against some Gram Positive
(4 th Generation) & expanded Gram Negative.
- Used for Severe Community
acquired infection.
- Imipenem - Inhibit bacterial cell wall
β-lactams - Meropenem synthesis.
Carbapenems - The broadest spectrum of
Antibiotic activity among antibiotics:
most Gram Positive & most
Gram Negative, &
anaerobes
- Aztreonam - Inhibit bacterial cell wall
β-lactams synthesis.
Monobactams - Activity against Gram
Antibiotic negative only
 - Streptomycin - Interfere with bacterial
- Gentamycin protein synthesis by binding
to ribosomes and inhibiting
- Tobramycin them (Bacteriostatic).
- Neomycin - At high concentrations they
Aminoglycosides - Netilmicin interfere with the cell wall
Antibiotic (Bactericidal).
- Amikacin

- Norfloxacin - Inhibit bacterial DNA

(1 st Generation) synthesis by inhibiting DNA
gyrase, required for normal
- Ciprofloxacin and
DNA transcription and
ofloxacin duplication.
(2 nd Generation) - Also inhibiting
topoisomerase IV,
- Gatifloxacin,
interfering with the
Fluoroquinolones Gemifloxacin, separation of replicated
Antibiotic Moxifloxacin. chromosomal DNA during
cell division.
(3 rd Generation)
- Bactericidal.
- Exhibit post-antibiotic
effects: bacterial growth
inhibition continues even if
concentration<MIC
(minimal inhibitory
concentration).
- Erythromycin - Inhibit protein synthesis by
- Clarithromycin preventing translocation of
the 50S subunit of the
- Azithromycin
Macrolides Antibiotic bacterial ribosome along the
mRNA
- Bacteriostatic, but may be
bactericidal in high
concentrations against some
organisms.
 - Metronidazole (Flagyl) - Binding to DNA causing its
breakage.
Other Antibiotic - Antibiotic (only against
anaerobic bacteria).
- Antiparasitic
(Trichomoniasis, amebiasis,
giardiasis).
- Glibenclamide - Stimulate insulin release
Insulin Secretagogues - Gliclazide from pancreas.
Sulfonylureas - Increase tissue sensitivity to
insulin.
- Decrease hepatic glucose
output
- Metformin - Decreases hepatic glucose
production.
- Increases insulin sensitivity
(Increases peripheral
Insulin Sensitizers glucose uptake).
Biguanides - Decreases intestinal
absorption of glucose.
- Decreases LDL and VLDL
and increases HDL (Modest
effect).
- Pioglitazone - Increase the sensitivity of
Insulin Sensitizers - Troglitazone cells to insulin.
Glitazones
(Withdrawn)
(Thiazolidinedione)
- Rosiglitazone
(Withdrawn)
- Acarbose (Glucobay) - Inhibit pancreatic α-amylase
(inhibit breakdown of starch
to oligosaccharides).
- Irreversibly inhibit α-
α-Glucosidase Inhibitors glucosidase in the intestine
(so inhibits digestion of
oligosaccharides to
glucose).
- Decrease glucose
absorption.
 - Canagliflozin - SGLT2 reabsorbs most of
- Dapagliflozin the glucose filtered by the
Sodium Glucose kidney.
co-transporter 2 - Gliflozins inhibits SGLT2,
(SGLT2) Inhibitors reducing renal reabsorption
of glucose resulting in
increased glucose excretion
and lowering of plasma
glucose concentration.
- Liraglutide - Increase glucose-stimulated
(Glucagon Like Peptide) insulin secretion.
GLP-1 Receptor - Reduce hepatic
Agonists gluconeogenesis by
suppression of glucagon
secretion.
- Sitagliptin - Increase insulin secretion,
(Glucose Dependent - Vildagliptin reduce glucagon secretion,
Insulinotropic Peptide) and improve glycaemic
DPP-4 Inhibitors control.

- Levodopa +Carbidopa - L- dopa is A prodrug

converted to dopamine in
the substantia nigra
(dopamine does not cross
the BBB).
- A dopa decarboxylase
inhibitor that decreases
metabolism of L-dopa in the
Antiparkinsonian Drugs GIT and peripheral tissues
thus: Increases availability
of L-dopa to the CNS,
lowers the dose of L-dopa
needed by 4 to 5 fold, and
decreases severity of SE of
L-dopa.
- Carbidopa does not cross the
BBB therefore cannot
inhibit dopa decarboxylase
enzyme in the CNS.
 - Selegiline - Inhibit DA degradation to
Antiparkinsonian Drugs increase action of DA in the
MAO-B Inhibitor CNS

- Bromocriptine - works by increasing the

release of dopamine in the
- Amantadine
brain, amantadine replaces
some of the lost dopamine
and therefore reduces some
Antiparkinsonian Drugs of the symptoms of the
DA Agonists disease. Amantadine also
has a mild anticholinergic
effect. This means it
prevents the activity of a
neurotransmitter called Ach.

- Benztropine - works by blocking a certain

natural substance (Ach) to
Antiparkinsonian Drugs help to decrease symptoms
in people with PD.
Anticholinergics

- Clozapine - Blockage of 5-HT receptors.

- Olanzapine
Antipsychotics
- Risperidone
Atypical

- Chlorpromazine - Blockage of D2 receptors.

- Prochlorperazine
Antipsychotics
- Haloperidol
Typical

- Fluoxetine - Inhibit reuptake of 5-HT.

Antidepressants - Citalopram
SSRI (Selective
Serotonin Reuptake
Inhibitors)
 - Venlafaxine - Inhibit the reuptake of NE
Antidepressants and 5-HT.
SNRI (Serotonin
Norepinephrine
Reuptake Inhibitors)

- Imipramine - Inhibit the reuptake of NE

Antidepressants - Amitryptiline and 5-HT.
TCA (Tricyclic - Blocks muscarinic,
- Clomipramine
Antidepressants) histaminic and α adrenergic
receptors.

- Tranylcypromine - monoamine oxidase

enzymes are responsible for
breaking down
neurotransmitters such as
Antidepressants dopamine, NE and serotonin
MAO Inhibitors in the brain. MAOIs
(Monoamine Oxidase Increase the concentration
Inhibitors) of these three
neurotransmitters by
blocking the effects of
monoamine oxidase
enzymes.
- Mirtazipine - Blocks 5-HT2 and α2
Antidepressants receptors.
Atypical Agents

- Lithium - Works by changing the

release of chemicals in the
brain.

Other Antidepressants
 - Phenytoin - Block Initiation of Electrical
- Carbamazepine Discharge from focal area
OR Prevent Spread of
- Valproic Acid Abnormal Electrical
- Ethosuximide Discharge to adjacent brain
- Benzodiazepines(BDZ) areas by:
1. Blocking voltage gated Na+
like Diazepam
and Ca++ channels.
Antiepileptics 2. Enhancing inhibitory action
of GABA (an inhibitory
neurotransmitter).

- Interfering with the

excitatory action of
Glutamate (an excitatory
neurotransmitter).

- Alprazolam - Sedative hypnotics act by

- Diazepam making nerve cells less
excitable.
- Midazolam
- BDZ and Barbiturates bind
to the GABA receptor
complex causing Increased
opening & entry of chloride
into the neuron’s chloride
Anxiolytics channels. Also, it makes
Benzodiazepines (BDZ) neuron becomes
hyperpolarized (more
negative) and less
responsive to stimuli. This
produces anxiolytic,
sedative, and hypnotic
effects.
 - Phenobarbital - Sedative hypnotics act by
- Thiopental making nerve cells less
excitable.
- BDZ and Barbiturates bind
to the GABA receptor
complex causing Increased
Anxiolytics opening & entry of chloride
Barbiturates into the neuron’s chloride
channels. Also, it makes
neuron becomes
hyperpolarized (more
negative) and less
responsive to stimuli. This
produces anxiolytic,
sedative, and hypnotic
effects.
- Buspirone

Other Anxiolytics ----