JIACM 2004; 5(3): 259-65
REVIEW ARTICLE
Platelet Glycoprotein IIb/IIIa Receptor Inhibitors –
Role in Coronary Artery Disease
NS Neki*
Abstract
Gp IIb/IIIa receptor antagonists are potent antiplatelet agents since they block the final pathway in platelet aggregation triggered by
endogenous platelet activators. They include agents with varying pharmacodynamic and pharmacokinetic properties. More than 80%
inhibition of platelet aggregation is required for effective platelet activity. These drugs have emerged as a valuable adjunct for coronary
intervention (PTCA or Stenting) or acute coronary syndromes1.
Introduction
Glycoprotein IIb/IIIa receptors present on the surface,
numbering about 50-60 thousand per platelet, are
responsible for final pathway of platelet aggregation. This
platelet aggregation leads to acute vessel closure during
percutaneous coronary intervention (PCI), acute coronary
syndromes (ACS), acute myocardial infarction (AMI), and
restenosis by producing platelet derived growth factor.
Gp IIb/IIIa receptors belong to a class of integrins with a
specificity for binding to fibrinogen. These receptor
blockers have emerged as a valuable adjunct in
interventional cardiology. Blocking of these integrin
receptors interferes with the final common pathway of
platelet aggregation which is mainly responsible for acute
coronary syndromes1,2.
Classification of GPI
1. Naturally occurring peptide inhibitors (isolated
from Viper venoms and Puff adder) – are not used
clinically. Examples are (a) Trigramin, (b) Barbourin,
(c) Kistrin.
2. Synthetic inhibitors – are of 3 types:
i. Monoclonal antibodies: (a) Abciximab –
parenteral use; (b) YM337 – parenteral use.
ii. Peptide: Eptifibatide – parenteral use.
iii. Non-peptide: (a) parenteral use, e.g., tirofiban,
lamifiban, fradafiban; (b) Oral use, e.g., xemlofiban,
orofiban, sibrafiban, lefradafiban, roxifiban,
lotrafiban.
* Professor, Department of Medicine, Government Medical College/GND Hospital, Amritsar-143 001 (Punjab).
Gp IIb/IIIa inhibitors like abciximab, eptifibatide,
tirofiban, and lamifiban have been approved by FDA
for clinical use.
Abciximab
It is available since 1995 under the brand name of
ReoPro (R). It is a human-murine chimeric monoclonal
antibody fragment (C7E 3 Fab), a large molecule with
low dissociation constant and blocks the glycoprotein
IIb/IIIa moiety. It binds to vitronectin receptor which is
concerned with cell adhesion, migration, and
proliferation. Its plasma half life is short, i.e., 15-30 min.
and biological half life prolonged, i.e., 6-12 hrs or more.
There is 50-60% platelet blockade even 24 hrs. after
its administration. By way of protease degradation, free
circulation abciximab in the plasma is rapidly
eliminated. Its molecular weight is 47.6 KD (Kilodalton).
Its route of excretion is unknown.
Dosage schedule for (a) PCI:0.25 mg/kg bolus dose
followed by 0.125 ug/kg/min infusion over 12 hrs
(maximum 10 ug/min); (b) Unstable angina: 0.25 mg/
kg bolus dose followed by 10 ug/min, infusion over 18-
24 hrs before PCI and continued 1 hr after PCI.
Eptifibatide
It is available as intergrilin since 1998. It is a cyclic
heptapeptide which has the Lys-Gly-Asp (KGD) amino
acid sequence. Its molecular weight is 0.832KD and is
mainly excreted through kidneys and to some extent
through liver. So it is advisable to adjust the dose in
patients with renal insufficiency. Although it has high ischaemic syndromes without persistent ST
selectivity for Gp IIb/IIIa receptors, it does not bind to segment elevation (Table I).
other intergrin receptors. It has a plasma half life of
In the PARAGON trial using lamifiban, no statistical
2.5 hrs. Platelet aggregation is expected to be about
benefit was seen on acute ischaemic outcomes at
70% of normal 4 hrs after cessation of eptifibatide
30 days although there was significant reduction
infusion. Dosage schedule for (a) PCI: 135 ug/kg bolus
in death and myocardial infarction (MI) at 6 months
dose followed by 0.5 µg/kg/min. infusion over 20-24
in patients receiving low dose lamifiban and
hrs. (IMPACT II dose); (b) ACS: 180 ug/kg bolus dose
heparin5. In the PRISM trial using tirofiban, there
followed by 2 ug/kg min. infusion over 72-96 hrs.
was 36% reduction in combined endpoint of death,
(PURSUIT dose)3.
MI, or refractory ischaemia at 48 hrs and significant
reduction in death rate at 30 days6. But in the
Tirofiban
PRISM-PLUS trial using tirofiban with heparin, there
It is available as Aggrastat since 1998. It is a tyrosine was 28% reduction in endpoint of death at 7 days
derivative non-peptide mimetic with a half life of 2-2.5 which was maintained at 30 days7. In the PURSUIT
hrs. Its molecular weight is 0.495KD and 39-69% is excreted trial using eptifibatide8,9, there was significant
through kidneys. Dosage schedule for ACS is 0.4 ug/kg/ reduction from 9.1 to 7.6% in combined endpoint
min. bolus dose over 30 min. followed by 0.1 µg/kg/min. of death, non-fatal MI at 72 hrs which was
infusion over 48-96 hrs. maintained upto 30 days and six months
thereafter.
Lamifiban
2. Role in stable angina with PCI: In the Canadian
It is non-peptide mimetic with a half life of 2-2.5 hrs. Lamifiban study10, patients with unstable angina
Dosage schedule for ACS is 300 ug bolus dose followed showed significant reduction (p < 0.05) in the
by 1 ug/min. infusion over 72-120 hrs. incidence of death or non-fatal MI or need for
Pharmacological differences between abciximab versus urgent revascularisation during infusion period
peptide and non-peptide Gp IIb/IIIa receptor inhibitors. upto 5 days. In the EPISTENT trial11, use of
abciximab with stent has shown reduction in
Characteristics Abciximab Peptide and
mortality by 58% among stented patients. But with
non-peptide
combined stenting and abciximab use, the
Molecular wt. High Low reduction in mortality was more than 50% among
Half life Long (7hrs.) Short (2.5 hrs.) diabetic patients. In the EPIC trial using
Affinity for Gp Strong Weak abciximab12, 2099 high risk patients of unstable
IIb/IIIa receptors Strong Weak angina and or non-Q-wave MI < 12 hrs of onset of
Avidity of binding Strong Weak symptoms, clinical or angiographic characteristic
Specificity of binding Non-specific Specific predictive of high risk for ischaemic complications
were included. There was reduction in the primary
Immunogenecity Yes No
composite endpoint at 30 days from 12.8% in the
Effect on vitronectin Inhibition No effect
placebo to 8.3% in abciximab bolus and infusion
which was 4.5% at 30 days and 6.1% at 3 years. In
Clinical uses the EPILOG trial13 using abciximab, there was
1. Unstable angina without PCI (ACS): They are reduction in ischaemic complications by 55% at 30
indicated in ACS to reduce peri-procedural days with the use of heparin in all patients
complications. There have been 4 placebo undergoing angioplasty. In the CAPTURE trial14
controlled trials which have established the involving 1265 patients of refractory unstable
efficacy of these agents in patients of unstable angina, which were subjected to angiography

260 Journal, Indian Academy of Clinical Medicine
Vol. 5, No. 3
July-September, 2004
 followed by infusion of abciximab or placebo for
18-24 hours before PCI continuing until 1 hour
after completion of the procedure. There was
reduction in primary composite endpoint at 30
days from 15.9% in placebo group to 11.3% in
abciximab group. In the ADMIRAL trial involving
300 patients of AMI who underwent primary PCI
with or without abciximab15, there was reduction
in primary composite endpoint of death, MI, or
urgent revascularisation at 30 days, 6% in
abciximab group and 14.6% in placebo group (p =
0.01). At 6 months, corresponding figures were
7.4% and 15.9% (p = 0.02). TIMI 3 flow was
observed quite significantly in abciximab group.
Thus the benefit of abciximab persisted upto 6
months15.
In the CADILLAC trial involving 2081 AMI patients16,
they were randomised into 4 groups namely
primary PCI, primary PCI with abciximab, primary
stenting, and primary stenting with abciximab. It
was observed that normal flow was restored in the
target vessel in 94.5 to 96.9% of patients and at 6
months, the primary endpoint occurred in 20% of
patients after PTCA, 16.5% after PTCA plus
abciximab, 11.5% after stenting, and 10.2% after
stenting plus abciximab (p < 0.001). There were no
significant differences among the groups in the
rates of death, stroke, or re-infarction.
3. Role in AMI-facilitated thrombolysis: Although
fibrinolytic therapy is the mainstay of treatment
of AMI, yet it has many limitations including (a)
patients reporting late (> 12 hrs) after onset of
symptoms (b) risk of bleeding including
intracranial bleed (c) failure to achieve complete
reperfusion of occluded artery (d) chances of re-
occlusion in 5-10% of patients. Now, Gp IIb/IIIa
inhibitors are used as an adjunct to thrombolytic
therapy in the management of AMI. In IMPACT II
trial using eptifibatide, various workers17 found
TIMI-grade-3 coronary flow at 90 min. in 60% of
those receiving highest doses of eptifibatide plus
tPA (in placebo group only 39%). In RESTORE trial
using tirofiban18, there was significant reduction in
ischaemic outcomes and marked improvement in
Journal, Indian Academy of Clinical Medicine
Vol. 5, No. 3
patients. In TIMI 14 trial19, 72% patients treated with
50 mg alteplase plus abciximab had TIMI 3 flow in
57% patients but combination of streptokinase
and abciximab had lower rates of TIMI 3 flow and
higher rate of major bleeding complications. The
use of GP IIb/IIIa inhibitors and streptokinase was
not as effective as tPA and Gp IIb/IIIa inhibitors. In
addition, there was increased risk of moderate and
severe bleeding with this combination. TIMI trial19
showed that abciximab is a potent and safe
addition to reduced dose thrombolytic regimen for
ST segment elevation MI. The most promising
regimen was 50 mg of alteplase producing a 75%
rate of TIMI flow at 90 min. TIMI-3 flow rate was
significantly higher in the 50 mg alteplase plus
abciximab group versus alteplase only group at 60
min and 90 min. The rate of major haemorrhage
was 6% in patients receiving alteplase alone, 3%
with abciximab alone, 10% with streptokinase plus
abciximab, 7% with 50 mg of alteplase plus
abciximab and low dose heparin, and 1% with 50
mg alteplase with very low dose heparin. Thus,
abciximab facilitates the rate and extent of
thrombolysis that there is marked increase in TIMI
3 flow when combined with half the usual dose of
alteplase and this occurred without increased risk
of major bleeding. Modest improvements in TIMI
3 flow were seen when abciximab was combined
with streptokinase but it was associated with
increased risk of haemorrhage19. In TAMI 8 trial24,
abciximab was given after administration of
alteplase. It was observed that TIMI 2 or 3 flow was
achieved in 92% patients treated with abciximab
and 56% patients treated without abciximab.
Other uses of Gp IIb/IIIa inhibitors are:
4. In combination with alteplase, these inhibitors are
being evaluated in ischaemic stroke.
5. Their use in peripheral arterial thrombolysis is under
investigation.
6. PCI in diabetic patients: GP IIb/IIIa inhibitors have
equal or better efficacy in diabetic than non-diabetic
patients. In the PRISM PLUS trial involving 362 diabetic
patients and 1208 non-diabetic patients7, there was

July-September, 2004 261
 reduction in cumulative endpoints of death, MI, high dose lamifiban in PARAGON trial. However, there
refractory ischaemia or re-hospitalisation for unstable was significant bleeding with high dose lamfiban in
angina in diabetic patients at 7 days from 21.8% in PARAGON trial5 and with eptifibatide in PURSUIT trial8.
the heparin group to 14.8% in the heparin and
3. Thrombocytopenia: Acute severe thrombocy-
tirofiban group whereas the cumulative endpoints
topenia (platelet < 20000/m3)12,14 occurs because of
reduced from 16.7% to 12.4% in non-diabetic group.
immune mechanism. The risk is 0.4 to 1.1 with
In the EPISTENT trial11 abciximab treatment resulted
abciximab, 0-0.2% with eptifibatide, 0.1-0.3% with
in significant reduction (51%) in target vessel
tirofiban and 0-0.1% with lamifiban. Acute severe
revascularisation at 6 months in stented diabetic
thrombocytopenia develops within 24 hrs in 0.7% of
patients as compared to stented diabetic patients
patients using abciximab and it is a life threatening
receiving placebo. In the EPILOG trial13, treatment with
condition. Its treatment is discontinuation of drug and
the use of abciximab resulted in lower adverse effects
platelet transfusion.
after PCI in both diabetics and non-diabetics.
4. Immunogenicity: It is seen in 5-6% of patients with
Side effects/complications of GPI: abciximab. However, Reopro Readministration
1. Bleeding complications: In the EPIC trial involving Registry (R3)21 has shown that its re-administration is
abciximab12, the risk of bleeding was high but in equally effective as first time administration with
the EPISTENT and EPILOG trial11, 13, the risk of similar risks.
bleeding was low on account of low dose as well
5. Effect on restenosis: In the EPIC trial12, the incidence
as weight adjusted dose of heparin and earlier
of ischaemia driven target vessel revascularisation
sheath removal. Even in TIMI 14 trial19, addition of
(TVR) at 6 months was 16.5% in the drug group
abciximab with reduced dose alteplase did not
compared to 22.3% in placebo. In the EPILOG (18.1%
result in increased bleeding. In patients who
Vs 16.6%), and CAPTURE (25.9% Vs 25.8%) trials13,14,
develop refractory or life threatening bleeding, the
no difference in TVR was found. Tirofiban in the
antiplatelet effect of abciximab may be reversed
RESTORE trial (15.7% Vs 17.1%)18 and eptifibatide in
by discontinuation of drug infusion and by platelet
the IMPACT II trial (20.9% Vs 20.7%)22 also did not
transfusion after 10-30 min, required for clearance
reduce restenosis rates. Restenosis is mainly due to
of circulating drug. After transfusion of platelets,
neointimal proliferation23.
abciximab redistributes from old to new platelets
reducing the mean level of receptor blockade.
Contraindications25-27
Platelet infusion is rarely required with the use of
rapidly reversible agents like eptifibatide and
Active internal bleed
tirofiban. Normal homoeostasis should be restored
History of bleeding diathesis
within 2-3 hrs of discontinuation. Emergency
Severe uncontrolled hypertension
bypass surgery is not complicated by excessive

Hypersensitivity reactions
bleeding even in the presence of prolonged Gp IIb/
IIIa inhibition20. The initial trials involving Gp IIb/
Platelet count < 1 lac/mm3
IIIa receptor antagonists showed higher rate of
History of intracranial bleed, intracranial neoplasm, AV
bleeding but subsequently it was shown to be due malformations, or aneurysm
to excessive and prolonged simultaneously
History of CVA within 1 year or haemorrhagic stroke
heparin administration. at any time

2. Haemorrhagic risk: Intracranial haemorrhage was
History of vasculitis (Abciximab)

not reported with any GPI. But there was significant
Acute pericarditis (Tirofiban)
bleeding with eptifibatide in PURSUIT trial and with
S. Creatinine > 4 mg/dl (Eptifibatide, Tirofiban).

262 Journal, Indian Academy of Clinical Medicine
Vol. 5, No. 3
July-September, 2004
Table I : Studies of Gp IIb/IIIa inhibitors in unstable angina4.
Study Number Bolus dose Infusion Duration Primary endpoint
of pts. µg/kg dose/min
Lamifiban (PARAGON) 2,282 300-750 1-5 ug 72.120 30 Days death/MI
Tirofiban (PRISM-) 3,231 18 0.15 ug/kg 48 48 hrs death/MI/refractory
angina
(PRISM-PLUS) 1,915 0.6 0.15 ug/kg 48-60 30 Days death/MI/refractory
0.4 ischaemia
Eptifibatide 10,948 180 1.3 ug/kg 72 30 Days
(PURSUIT) 180 2.0 ug/kg Death/MI

Table II : Approved dosing and adminstration guidelines for Gp IIb/IIIa receptor inhibitors4.
Study Number Loading Infusion Duration Primary end Indication
dose ug/kg dose/min hrs. point at 30 days
Abciximab
EPIC 2,099 250 10 µg 12 Death/MI, High risk for
revascularisation abrupt closure
EPILOG 2,792 250 0.125 12 Death/MI, urgent Elective/urgent
µg/kg revascularisation intervention
CAPTURE 1,265 250 10 µg 17-24 Death/MI/recurrent/ Intervention for
ischaemia with urgent unstable angina
revascularisation
Eptifibatide
IMPACT II 4,010 135 0.5 U 20-24 Death/MI/urgent Any PCI
µg/kg revascularisation
Tirofiban 2,141 10 0.15 36 Death/MI/ Intervention with
µg/kg revascularisation 72 hrs of unstable
angina or MI
Table III : Showing clinical events of death, MI, or urgent revascularisation at 31 days.
Treatment group Placebo % (n) GP IIb/IIIa % (n) P value
EPIC
Abciximab B 12.8% (696) 11.4 (695) 0-4300
Abciximab B+1 12.8% (696) 8.3% (708) 0.008
EPILOG
Abciximab LDH 11.7% (939) 5.2% (935) < 0.001
Abciximab SDH 11.7% (939) 5.4% (918) < 0.001
EPISTENT
Abciximab + stent 10.8% (809) 5.3% (794) < 0.001
Abciximab + PTCA 10.8% (809) 6.9% (796) 0.007
IMPACT III
Eptifibatide 11.4% (1328) 9.2% (1249) 0.063
Eptifibatide 11.4% (1328) 9.9% (1333) 0.220
RESTORE
Tirofiban 10.5% (1070) 8.0% (1071) 0.052
CAPTURE
Abciximab 15.9% (635) 11.3% (630) 0.012
RAPPORT
Abciximab 11.2% (242) 5.8% (241) 0.030

Journal, Indian Academy of Clinical Medicine
Vol. 5, No. 3
July-September, 2004 263
Table IV : Showing clinical events of death, MI, or urgent revascularisation at 6 months31.
Treatment group Placebo % (n) GP IIb/IIIa inhibitor % (n)
EPIC
Abciximab B 12.8% (696) 10.2% (695)
Abciximab B+1 12.8% (696) 8.9% (708)
EPILOG
Abciximab LDH 11.1% (939) 6.3% (935)
Abciximab SDH 11.1% (939) 5.6% (918)
EPISTENT
Abciximab + stent 11.4% (809) 5.6% (794)
11.4% (809) 7.8% (796)
IMPACT III
Eptifibatide 11.6% (1328) 10.5% (1349)
Eptifibatide 11.6% (1328) 10.1% (1333)
RESTORE
Tirofiban 8.6% (1070) 7.8% (1071)
CAPTURE
Abciximab 10.9% (635) 9.0% (630)
RAPPORT
Abciximab 11.2% (242) 8.7% (241)

Oral Gp IIb/IIIa inhibitors
Various trials28-30 have shown greater bleeding as well as
greater mortality rate with the long term use of oral GpIIB/
IIIa inhibitors like xemilofiban, sibrafiban, and orofiban. The
exact cause of increased bleeding rates with these drugs
in unclear but paradoxical receptor activation theory has
been proposed. Thus oral GPI have no role in PCI.
Drawback of Gp IIb/IIIa inhibitors is their higher cost.
Conclusion
GpIIb/IIIa receptor inhibitors differ in their
pharmacodynamic and pharmacokinetic properties. The
beneficial effects of these agents have been shown at 6
months and 1 year of follow up. Intravenous GpIIb/IIIa
inhibitors undoubtedly serve as important clinically
effective adjunct therapy during PCI (PTCA or Stenting)
and in the management of patients with ACS. Various trials
conducted so far have shown the superiority of abciximab
over small molecules in preventing thrombotic events,
reducing the primary end points at 30 days in PCI as well
as reducing the hospital stay of patients. Still more data is
required to judge the superiority of large versus small
molecules in various clinical settings.
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