1. Dr. RAGHU PRASADA M S
MBBS,MD
ASSISTANT PROFESSOR
DEPT. OF PHARMACOLOGY
SSIMS & RC.
1

4. ADP receptor blocker
CLOPIDOGREL
TICLOPIDINE
COX
inhibitor
(Aspirin)
Phosphodiesterase
inhibitor-
DIPYRIDAMOLE,
CILOSTAZOLE
Gb IIb/IIIa
receptor
blockers
ABCIXIMAB
EPTIFIBATIDE
TIROFIBAN
TXA2 receptor
TERUTROBAN

5. Aspirin
N.B.Aspirin inhibitsThromboxane A2 & prostacyclin too, but the former is more
affected because platelets don’t have nuclei can’t synthesize new enzymes for
next 7 daysplatelets life span

6.  Most authorities recommend initial therapy
with a dose of 160 mg (one half-tablet) to 325
mg (one adult tablet)
 Aspirin should be crushed/chewed (to
facilitate faster absorption by breaking the
enteric-coated delayed release tablet

7.  Prophylaxis against unstable angina
 Post MI
 Post stroke
Adverse effects
GI –ulceration
Prolonged bleeding time  ↑ risk of hemorrhage

8. ABCIXIMAB is composed of 7E3 Fab fragments.
derived from murine (mouse)
 Humanised monoclonal antibody.
 directed against glycoprotein receptor type GPIIb/IIIa.
 Mechanism: The m7E3 Fab binds selectively to the
glycoprotein GPIIb/IIIa receptors inhibiting platelet
aggregation
 Plasma T1/2- 30min
 Bolus –followed by slow IV infusion
 Major side effect- bleeding

9. TIROFIBAN -non-peptic
 Synthetic arginine-glycine-aspartic acid (R-G-D)
sequence mimetics
 Hence, it blocks the binding of fibrinogen to
glycoprotein GPIIb/IIIa receptors
 They are given intravenously for the reduction of
thrombotic complications during coronary angioplasty
(if they are given orally they are toxic)
 Clinical trials showed reductions in the incidence of
death and non-fatal MI in response to the use of
tirofiban.

10. TICLOPIDINE & CLOPIDOGREL
They inhibit irreversibly ADP binding to receptors 
inhibit platelet aggregation
No effect on PG synthesis
Used in aspirin intolerant patients

11.  Acts by in inhibiting phoshodiesterase enzyme
 Incompletely absorbed from the gastrointestinal
tract with peak plasma concentration occuring
about 75 minutes after oral administration
 More than 90% bound to plasma proteins
 A terminal half-life of 10 to 12 hours
 Metabolised in the liver
 Mainly excreted as glucuronides in the bile;
a small amount is excreted in the urine

12.  It is an inhibitor of phosphodiesterase III (PDE III)
enzyme
 Vasodilator and inhibitor of platelet aggregation
 Intermittent claudication
 Indicated for the reduction of events (myocardial
infarction, stroke, and vascular death) in patients
with atherosclerosis documented by recent stroke,
recent MI or established peripheral arterial disease
 C/I- CHF patients

13. Prasugrel
Thienopyridine
More rapid onset of action than clopidogrel
Irreversible inhibitor of the P2Y12 receptor
Beneficial in the treatment and prevention of ACS
and the prevention of thromboembolic events
Adenosine Diphosphate-Receptor Antagonists

14. Ticagrelor
Cyclo-pentyl-triazo-pyrimidine (CPTP)
More rapid onset of action than clopidogrel
Reversible inhibitor of the P2Y12 receptor

15.  Myocardial infarction
 Unstable angina
 Coronary bypass implants
 Prosthetic heart valves and arteriovenous shunts
 Venous thromboembolism and PVD
 Cerebrovascular transient ischemic attacks

16. Streptokinase
Urokinase
Anistreplase
t-PA
Reteplase
tenecteplase

20.  1ST GEN:
 STREPTOKINASE (SK)
▪ Derived from ß-hemolytic streptococci
▪ Binds & activates plasminogen plasmin “systemic”
fibrinolysis
▪ 1-1.5 million U IV over 60min
▪ Cheap
 ANTISTREPLASE (plasminogen-SK)
▪ 30mg IV over 5 min
*Allergic reactions (6%)
*Avoid re-treatment for 6 months (+Ab)

21.  2ND GEN: ALTEPLASE (TPA)
 Cleaves plasminogen plasmin fibrinolysis
 Specific activity in thrombus, less systemic
fibrinolysis
 Weight-based IV infusion over 60-90min
 Half-life<5 min
 Heparin commonly administered shortly after

22.  3RD GEN: modifications of TPA
 RETEPLASE
▪ Half-life= 18 min
▪ Double bolus regimen
 TENECTEPLASE (TNK)
▪ Half life= 20 min
▪ Single-weight tiered bolus dosing over 5-10s
* No absolute mortality benefit in AMI

23.  The plasma half-life of the third generation drugs is
14-45 minutes, allowing administration as a single or
double intravenous bolus.
 This is in contrast to second generation t-PA, which
with a half-life of 3-4 minutes, must be administered
an initial bolus followed by infusion

24.  Coronary Thrombolytics
 Pulmonary embolism
 DVT
 Arterial occlusion e.g. Popliteal artery
 Ischaemic stroke
 Occluded AV shunts
 Blocked central vacuum catheters

25.  Intracranial hemorrhage or hemorrhagic stroke
 Ischemic Stroke within 3 month
 Known structural cerebrovascular lesion (AVMs,
aneurysms, tumor)
 Closed head injury with in 3 months.
 Aortic dissection
 Severe uncontrolled hypertension SBP > 180 DBP >
110
 Active bleeding or bleeding diathesis
 Acute pericarditis