ALI, JANNA-IZZA B.

BATCH 2023
NEURO 1 MODULE

DRUG COMPENDIUM

ASPIRIN
Generic name: Aspirin
Drug class: Salicylates, Anticoagulants & Fibrinolytics (Thrombolytics)
General Chemistry:

DESCRIPTION

-It is a selective and irreversible inhibitor of cyclooxygenase-1 (COX-1) enzyme resulting in

MECHANISM OF ACTION direct inhibition of the biosynthesis of prostaglandins and thromboxanes from arachidonic acid.

It exhibits analgesic, anti-inflammatory, and antipyretic activities.

CLINICAL EFFECTS It also inhibits platelet aggregation.

Fever, Rheumatic disorders, MI, Angina pectoris, Acute ischemic stroke, prophylaxis of
CLINICAL INDICATIONS cardiovascular events in high-risk patients

Absoprtion: Rapidly absorbed from the GI tract. Partially hydrolysed by esterases to salicylate
during absorption in the GI tract.
Bioavailability: 50-75%
Peak plasma levels: Approx 1-2 hours (nonenteric-coated); 3-4 hours (enteric-coated); Approx
2 hours (extended-release cap)
Distribution: Crosses the placenta and enters breast milk.
PHARMACOKINETICS
Volume distribution: 170 mL/kg
Plasma protein binding: 80-90%
Metabolism: Metabolized in the liver into salicyluric acid, salicyl phenolic glucuronide,
salicylic acyl glucuronide, gentisic acid, and gentisuric acid. Undergoes first-pass metabolism.
Excretion: Via urine (75% as salicyluric acid, 10% as salicylic acid)
Elimination half-lives: 15-20 minutes

Antiplatelet: 40-80 mg/d

Pain/Fever: 325-650 mg/4-6 h

For nonviral etiologies fever: 50-70 mg/kg/day in 4-6 divided doses, max of 3.6 g.
DOSAGE
Rheumatic Fever: 1g/4-6 h

Children: 10 mg/kg/4-6 h

-Hypersensitivity to aspirin or other NSAIDs, Peptic ulcer, Hemorrhagic disease, Coagulation

CONTRAINDICATIONS disorder (e.g. hemophilia, thrombocytopenia), Gout, Severe hepatic and renal impairment,
Children <16 years and recovering from viral infection
 Salicylate sensitivity, tinnitus, Anemia, hypoprothrombinemia, thrombocytopenia, Dyspepsia,
gastric irritation, nausea, vomiting, Dizziness, confusion, Asthma, bronchospasm, dyspnea,
rhinitis, Rash, urticarial
ADVERSE REACTION

CLOPIDOGREL
Generic name: Clopidogrel
Drug class: Antiplatelet drug
General Chemistry:

DESCRIPTION

- inhibit the binding of ADP to its receptors on platelets and, thereby, inhibit the activation of
MECHANISM OF ACTION
the GP IIb/IIIa receptors required for platelets to bind to fibrinogen and to each other

- reduce the rate of stroke, myocardial infarction,and death in patients with recent myocardial
CLINICAL INDICATIONS
infarction or stroke,established peripheral arterial disease, or acute coronary syndrome. 

Absorption: Rapidly but incompletely absorbed from the gastrointestinal tract (approx 50%).
Time to peak plasma concentration: Approx 45 minutes.
Plasma protein binding: 98% (parent drug); 94% (carboxylic acid derivative).
Metabolism: They undergo hepatic metabolism by the cytochrome P450 (CYP) system to
PHARMACOKINETICS active metabolites. 
Excretion: Elimination of the drugs and metabolites occurs by both the renal and fecal routes
Half-life: Approx 6 hours (parent drug); approx 0.5 hours (thiol derivative); approx 8 hours
(carboxylic acid derivative).
 

DOSAGE The usual dose is 75 mg/day with or without an initial loading dose of 300 or 600 mg

Active pathological bleeding (e.g. peptic ulcer or intracranial haemorrhage). Severe hepatic
CONTRAINDICATIONS
impairment.

ADVERSE REACTION prolonged bleeding

Thrombotic thrombocytopenic purpura 

WARFARIN
DESCRIPTION Generic name: Warfarin
Drug class: Anticoagulant (Vitamin K Antagonist)
General Chemistry:
 - Inhibit the production of vitamin K by vitamin K epoxide reductase.
MECHANISM OF ACTION

- Prophylaxis and treatment of venous thromboembolism and related pulmonary embolism;

CLINICAL INDICATIONS atrial fibrillation; cardiac valve replacement; Secondary prevention of stroke.

Absorption: Completely absorbed from the GI tract. The mean Tmax for warfarin sodium
tablets is 4 hours.
Distribution: Volume of distribution 0.14 L/kg; Protein binding: 99%.
Metabolism: Major metabolic pathway is oxidation to various hydroxywarfarins, comprising
80-85% of the total metabolites; minor pathway of metabolism is the reduction of the ketone
PHARMACOKINETICS
group to warfarin alcohols, comprising 20% of the metabolites.
Excretion: Almost entirely by metabolism with a small amount excreted unchanged; 80% of the
total dose is excreted in the urine with the remaining 20% appearing in the feces; Half-life for R-
warfarin is 37-89 hours. Half-life for S-warfarin is 21-43 hours.

DOSAGE 5-10 mg QD as starting dose.

Severe bleeding
Hemoptysis
ADVERSE REACTION black or bloody stool
joint pain

DABIGATRAN
Generic name: Dabigatran
Drug class: Direct Oral Thrombin Inhibitor
General Chemistry:

DESCRIPTION

- Dabigatran competitively and reversibly blocks the active site of free and clot-bound thrombin.
In turn, this blocks thrombin-mediated conversion of fibrinogen to fibrin, feedback activation of
MECHANISM OF ACTION
coagulation, and platelet activation.

-Treatment of acute venous thromboembolism after at least 5 days of parenteral anticoagulation

with heparin, LMWH, or fondaparinux
- Secondary prevention of venous thromboembolism
CLINICAL INDICATIONS - Stroke prevention in patients with nonvalvular atrial fibrillation
- Thromboprophylaxis after knee or hip arthroplasty (lower-dose regimens of once-daily
dabigatran)
 Administration: Taken orally twice a day in capsule
form
Bioavailability: 6% (altered if capsules are chewed or
broken prior to ingestion)
PHARMACOKINETICS Peak onset of action: 2 h
Half-life: 12-14 h
Plasma protein binding: 35%
Excretion: 80% excreted unchanged by kidneys

- Dosage reduction is required when administered to patients with severe renal impairment
(creatinine clearance 15-30 mL/min).
- Dosage recommendations are not available for patients with a creatinine clearance <15
DOSAGE
mL/min.

- Patients with mechanical heart valves

CONTRAINDICATIONS
- Bleeding
ADVERSE REACTION

BETAHISTINE
Generic name: Betahistine
Drug class: Antivertigo drugs
General Chemistry:

DESCRIPTION

- Betahistine is a histamine analogue. The exact mechanism is not yet fully determined;
however, it is known to act as both partial histamine H1-receptor agonist and histamine H3-
MECHANISM OF ACTION
receptor antagonist in neuronal tissue, with negligible histamine H2-receptor activity.

- For vertigo, tinnitus and hearing loss associated in patients with Meniere’s disease
CLINICAL INDICATIONS

Absorption:When given orally, betahistine is rapidly and almost completely absorbed from the
gastrointestinal tract.In the fasted state, Cmax is achieved within 1 hour of administration; in the
fed state, Cmax is delayed, but the total drug absorption is similar. Food, therefore, has little
effect on the absorption of betahistine
PHARMACOKINETICS Plasma protein binding: less than 5%.
Metabolism: metabolized primarily into the inactive metabolite 2-pyridylacetic acid.
Excretion: Betahistine is mainly excreted in the urine; with approximately 85-91% being
detected in urine samples within 24 hours of administration
Half-life: 3-4 hours

As betahistine dihydrochloride: Initially, 8-16 mg tid or 24 mg bid, adjusted according to

DOSAGE
individual response. Maintenance: 24-48 mg daily. Max: 48 mg daily.
As betahistine mesilate: 6-12 mg tid.
Salicylate sensitivity, tinnitus, Anemia, hypoprothrombinemia, thrombocytopenia, Dyspepsia,
gastric irritation, nausea, vomiting, Dizziness, confusion, Asthma, bronchospasm, dyspnea,
CONTRAINDICATIONS
rhinitis, Rash.

- nausea, upset stomach, vomiting, diarrhea and stomach cramping.

ADVERSE REACTION

CINNARIZINE
DESCRIPTION Generic name: Cinnarizine
Drug class: Antivertigo drugs, Peripheral Vasodilators & Cerebral Activators
General Chemistry:
 - inhibits contractions of vascular smooth muscle cells by blocking L-type and T-type voltage
gated calcium channels, thereby reducing free Ca ions available for the induction and
MECHANISM OF ACTION
maintenance of contraction.

- Motion Sickness
- Nausea and Vertigo caused by Meniere’s disease, Vertigo and vestibular disorders
CLINICAL INDICATIONS
- Cerebrovascular disorders
- Peripheral Circulatory Disorders
Absorption: slowly absorbed
Time to peak plasma concentration: 4 hours
Plasma protein binding: 91%
PHARMACOKINETICS Metabolism: Extensively metabolized mainly by cyp2d6.
Excretion: via feces (mainly as unchanged drug) and urine (as metabolites)
Half-life: 3-6 hours.

Motion Sickness
Adult: Initially, 30mg 2 hours before travel, then 15 mg 8 hourly during the journey if
necessary.
Child (5-12years old): 15 mg 2 hours before travel, then 7.5 mg 8 hourly during the journey if
necessary.
Nausea and Vertigo caused by Meniere’s disease, Vertigo and vestibular disorders
DOSAGE
Adult: 30 mg tid
Child (5-12 years old): 15 mg tid
Cerebrovascular disorders
Adult: 25 mg tid
Peripheral Circulatory Disorders
Adult: 50-75 mg bid to tid with Max: 225 mg daily

Hypersensitivity to Cinnarizine
CONTRAINDICATIONS
Children <5 years of age

- Epigastric discomfort
ADVERSE REACTION

CITICOLINE
Generic name: Citicoline
Drug class: Nootropics & Neurotonics/Neurotrophics
General Chemistry:

DESCRIPTION

- Citicoline is a naturally occurring endogenous nucleoside involved in the biosynthesis of

lecithin. It increases the synthesis of phosphatidylcholine (main neuronal membrane
MECHANISM OF ACTION
phospholipid) and enhances acetylcholine production. 

CLINICAL INDICATIONS - Cerebrovascular disorders

 - Cognitive disorder
- Head Injury
- Parkinson’s disease
Absorption: Rapidly absorbed in the gastrointestinal tract.
Bioavailability: >90%
Time to peak plasma concentration: 1 hour after oral administration followed by 2nd peak at
24 hours post-dosing.
PHARMACOKINETICS Distribution: Distributed throughout the body, crosses blood-brain barrier.
Metabolism: Metabolised in the liver and gut wall via hydrolysis to choline and cytidine
Excretion: Mainly via respiratory CO2
Half-life: 71 hours (urine); 56 hours (respiratory CO2)

- IM, IV: 500-1000mg daily given via IM inj or slow inj 3-5 minutes, or infused at a rate of 40-
DOSAGE 60 dpm.
- PO: As tab: 500 mg once daily or bid, or 1000 mg once daily. As solution: 100-200 mg bid or
tid.
Hypertonia of the parasympathetic nervous system.
CONTRAINDICATIONS

LOSARTAN
Generic name: Losartan
Drug class: Angiotensin Receptor Blocker (ARB)
General Chemistry:

DESCRIPTION

- It binds to AT1 receptors with much higher affinity than AT2 receptors. It blocks Angiotensin
MECHANISM OF ACTION in vascular smooth muscle and adrenal cortex.

ARB inhibits most of the biological effects of AngII, which include AngII-induced (1)
contraction of vascular smooth muscle; (2) rapid pressor responses; (3) slow pressor responses;
CLINICAL EFFECTS (4) thirst; (5) vasopressin release; (6) aldosterone secretion; (7) release of adrenal
catecholamines; (8) enhancement of noradrenergic neurotransmission; (9) increases in
sympathetic tone; (10) changes in renal function; and (11) cellular hypertrophy and hyperplasia
- Hypertension
CLINICAL INDICATIONS - Diabetic Mellitus nephropathy
- Stroke prophylaxis
Absoprtion: Well absorbed from the GI tract. Decreased absorption with food.
Bioavailability: 33%
Peak plasma levels of losartan and EXP 3174 occur about 1–3 hrs after oral administration.
Distribution: Volume distribution: 34 L.
PHARMACOKINETICS Plasma protein binding: >98%
Metabolism: it undergoes extensive hepatic first-pass metabolism and converted by CYP2C9
and CYP3A4 to 5-carboxylic acid metabolite, EXP 3174
Excretion: Via urine (35%) and feces.
Elimination half-lives: 2.5 hrs and 6–9 h (active metabolite)
DOSAGE 50 – 100 mg daily
- Concommitant use with aliskiren-containing products in patients with diabetes mellitus or
renal impairment.
CONTRAINDICATIONS
- Severe hepatic impairment
- Pregnancy
 - Renal failure,
- Symptomatic hypotension,
- Hyperkalemia,
ADVERSE REACTION - Angioedema