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Eptifibatide (Integrilin)8 residuesHARGDWPCEach bubble = one amino acid. Size = residue mass. Color = chemical class.Also known as: Integrilin
Rattlesnake venom inspired one of cardiology's most reliable antiplatelet drugs. Eptifibatide (Integrilin) is a cyclic heptapeptide that blocks the GP IIb/IIIa receptor, the final checkpoint in platelet clot formation. The PURSUIT trial tested it in 10,948 patients with acute coronary syndromes and confirmed a reduction in death and heart attack at 30 days. ESPRIT then showed a 37% relative risk reduction during coronary stenting. This is strictly a hospital IV drug; nobody self-administers eptifibatide. Interventional cardiologists reach for it during high-risk procedures because platelet function bounces back within 4 to 8 hours after stopping the infusion.
A seven-amino-acid loop borrowed from pygmy rattlesnake venom turned into one of the most widely studied antiplatelet agents in interventional cardiology. Eptifibatide, marketed as Integrilin and first approved by the FDA in 1998 (NDA 020718), is a synthetic cyclic heptapeptide derived from barbourin, a disintegrin protein found in Sistrurus miliarius barbouri. Its CAS number is 148031-34-9. The drug works by sitting in the ligand-binding pocket of the GP IIb/IIIa receptor on activated platelets. That receptor is the final common pathway for platelet aggregation, regardless of what triggered the platelet in the first place (thrombin, ADP, collagen, thromboxane A2). By blocking fibrinogen from bridging adjacent platelets, eptifibatide shuts down clot formation at the last step. Two large randomized controlled trials defined its place in practice. PURSUIT (NEJM 1998, n=10,948)[1] enrolled patients with non-ST-elevation acute coronary syndromes and tracked death or myocardial infarction at 30 days. The eptifibatide group came in at 14.2% versus 15.7% for placebo. ESPRIT (Lancet 2001, n=2,064)[2] focused on elective coronary stenting and landed on a 37% relative risk reduction in the composite of death, MI, and urgent target vessel revascularization at 48 hours. That benefit held at six months. Eptifibatide is given exclusively by IV in monitored hospital settings. Its pharmacokinetics are linear and dose-proportional, with a plasma half-life of about 2.5 hours. Platelet function returns to near-normal within 4 to 8 hours of stopping the drip. Around 50% of the drug clears through the kidneys, so patients with a creatinine clearance below 50 mL/min get a halved infusion rate.
Every platelet carries roughly 80,000 copies of the GP IIb/IIIa receptor (integrin alphaIIb-beta3) on its surface. When a platelet activates, whether from thrombin exposure, ADP release, collagen contact, or thromboxane A2, that receptor flips from a low-affinity to a high-affinity state. In its active conformation, GP IIb/IIIa grabs onto fibrinogen and von Willebrand factor. Those proteins then cross-link neighboring platelets into a growing thrombus. Eptifibatide is a cyclic heptapeptide built around a Lys-Gly-Asp (KGD) motif. That sequence was modeled after barbourin, a disintegrin from pygmy rattlesnake venom. KGD mimics the Arg-Gly-Asp (RGD) site that fibrinogen normally uses to dock onto GP IIb/IIIa. By occupying that binding pocket, eptifibatide keeps fibrinogen from bridging platelets together. The binding is reversible and competitive. That matters clinically. Compared to abciximab (a monoclonal antibody fragment that locks onto the receptor for hours), eptifibatide dissociates faster once the infusion stops. Platelet aggregation returns to near-baseline levels within 4 to 8 hours. At therapeutic plasma concentrations, receptor occupancy stays above 80%, which translates to greater than 80% inhibition of ADP-induced platelet aggregation. The ESPRIT double-bolus protocol (second 180 mcg/kg at 10 minutes) exists specifically to prevent an inhibition dip during the most dangerous window of a stenting procedure.
FDA-approved cyclic heptapeptide GP IIb/IIIa inhibitor with strong RCT evidence for ACS and PCI. PURSUIT trial (n=10,948) demonstrated significant reduction in death/MI at 30 days in NSTEMI/UA. ESPRIT trial showed 37% relative risk reduction in death/MI at 6 months for elective stenting. 2023–2025 literature explores adjunct use in acute ischemic stroke thrombectomy and STEMI primary PCI. ACC/AHA 2022 Chest Pain/ACS Guidelines retain Class IIa recommendation for high-risk NSTEMI patients undergoing PCI.
PURSUIT (PMID 9705684, NEJM 1998, n=10,948) for ACS; ESPRIT (PMID 11368699, Lancet 2001, n=2,064) for PCI/stenting
IV-only, hospital-administered exclusively: no outpatient or self-administration use. Renal dose adjustment required (CrCl <50 mL/min). Largely displaced by dual antiplatelet therapy (DAPT) in routine NSTEMI management since widespread use of potent P2Y12 inhibitors. Benefit attenuated in radial-access centers with very low baseline bleeding rates. No reversal agent.
Hospital-administered IV drug: no self-administration community exists. Clinical community (interventional cardiologists, cath lab pharmacists, critical care nursing) views eptifibatide as a niche but established tool for high-risk NSTEMI and elective PCI. Usage has declined since potent P2Y12 inhibitors (ticagrelor, prasugrel) became standard DAPT. Preferred over abciximab in most centers due to faster platelet function recovery (4–8h vs 12–24h) and lower profound thrombocytopenia risk.
Exclusively hospital-administered IV drug with no self-administration or consumer community. All dosing data derives from FDA label and RCTs. No lay-community protocols, forum discussions, or self-experimentation data exist for eptifibatide.
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 180 mcg/kg | Single dose |
| Moderate | 180 mcg/kg | Single dose |
| Aggressive | 180 mcg/kg | Double bolus (x2, 10 min apart) |
Eptifibatide comes ready to use. No reconstitution needed. Two vial concentrations exist: 2 mg/mL in a 10 mL bolus vial (20 mg total) and 0.75 mg/mL in a 100 mL infusion vial (75 mg total). Mixing up the two vials is a recognized medication error. For the weight-based math on a 70 kg patient: 180 mcg/kg equals 12,600 mcg (12.6 mg). From the 2 mg/mL bolus vial, that's 6.3 mL. The continuous infusion at 2 mcg/kg/min equals 140 mcg/min, which is 8.4 mg/h. From the 100 mL infusion vial (0.75 mg/mL), the rate comes to 11.2 mL/h. The mistake that trips up cath lab teams most often is flat-dosing instead of weight-based dosing. Writing "180 mcg" instead of "180 mcg/kg" underdoses by a factor of 70. Always confirm the calculation: dose equals the per-kg value times actual body weight in kilograms; use actual weight, not ideal. Store vials at 2 to 8 degrees Celsius, protected from light. Don't freeze. Use opened vials within 24 hours.
Eptifibatide is used acutely during PCI or ACS episodes and is not cycled. Administration typically lasts 18-72 hours per treatment event under hospital supervision. There is no ongoing or maintenance dosing regimen.
Eptifibatide is a single-event acute antiplatelet agent used during ACS hospitalization or PCI procedures. There is no cycling protocol: the drug is administered once per clinical event and cleared within 4–8h of infusion cessation due to its ~2.5h half-life and reversible competitive binding. The concept of on/off cycles, receptor desensitization, or axis recovery does not apply to an acutely administered IV platelet inhibitor.
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Expected: PURSUIT: 14.2% absolute rate of death/MI at 30 days vs 15.7% placebo (RRR ~10%); benefit concentrated in patients undergoing PCI. Onset of >80% platelet inhibition within minutes of bolus.
Monitor: CBC at baseline and within 6h of bolus; repeat daily. Hemoglobin and hematocrit monitoring for occult bleeding. Creatinine for infusion rate adjustment. ACT if co-administered with heparin (target 200–300 sec).
Confirm the patient has no contraindications: no active bleeding, no stroke within 30 days, no severe uncontrolled hypertension, no thrombocytopenia below 100,000/mm3, no major surgery within 6 weeks. Obtain baseline CBC, creatinine, and calculate CrCl using Cockcroft-Gault with actual body weight.
Calculate the bolus dose: 180 mcg/kg times actual body weight. For a 70 kg patient, that equals 12.6 mg. Draw 6.3 mL from the 2 mg/mL (10 mL) bolus vial. For an 80 kg patient: 14.4 mg, draw 7.2 mL.
Administer the bolus as IV push over 1 to 2 minutes through a dedicated line or compatible Y-site (normal saline or D5W).
For a 70 kg patient using the 0.75 mg/mL (100 mL) infusion vial, set the pump to 11.2 mL/h. If CrCl is below 50 mL/min, cut the rate to 1 mcg/kg/min (5.6 mL/h for a 70 kg patient).
For PCI (ESPRIT protocol): administer a second bolus of 180 mcg/kg exactly 10 minutes after the first. Do not skip this. The second bolus fills a receptor occupancy dip that single-bolus dosing leaves during the critical stenting window.
Continue the infusion for 18 to 24 hours post-PCI (minimum 12 hours) or up to 72 hours in medically managed ACS.
Check platelet count within 6 hours of the first bolus and daily thereafter. Monitor hemoglobin for occult bleeding. When heparin is co-administered, target an activated clotting time of 200 to 300 seconds.
Stop the infusion if platelets drop below 100,000/mm3, if a major bleeding event occurs, or when the maximum infusion duration is reached.
Standard co-administration per FDA label and RCT protocols. UFH provides anticoagulation while eptifibatide handles platelet aggregation inhibition. ACT target 200–300 sec when co-administered during PCI.
UFH 60 IU/kg bolus (max 5,000 IU) pre-PCI; titrate to ACT 200–300 sec. Stop heparin at end of PCI procedure; continue eptifibatide infusion.
DAPT co-administration is mandatory in ACS and PCI management. Aspirin COX-1 inhibition is complementary to GP IIb/IIIa blockade. All major eptifibatide RCTs included aspirin.
325 mg loading dose; 81 mg/day maintenance indefinitely post-stent.
P2Y12 inhibitor used in triple antiplatelet therapy with eptifibatide + aspirin for high-risk PCI per ESPRIT-era protocols. Additive platelet inhibition at different receptor targets.
300–600 mg loading dose pre-PCI; 75 mg/day maintenance (12 months post-stent).
More potent P2Y12 inhibitor preferred over clopidogrel in ACS per current ACC/AHA guidelines. Used alongside eptifibatide in high-risk NSTEMI/PCI where GP IIb/IIIa inhibitor is still employed.
180 mg loading dose; 90 mg twice daily maintenance.
Concurrent administration of two parenteral GP IIb/IIIa inhibitors is an FDA-labeled contraindication. No additive benefit; substantially increased bleeding and thrombocytopenia risk.
Do not combineSame receptor target as eptifibatide. Concurrent GP IIb/IIIa inhibitor use is contraindicated per FDA label: no benefit and increased hemorrhagic risk.
Do not combineMarkedly increased major hemorrhage risk. FDA label interaction. Pharmacoinvasive STEMI strategies combining thrombolytics with GP IIb/IIIa inhibitors show unacceptable intracranial bleeding rates.
Do not combineSubstantially elevated hemorrhagic risk from combined anticoagulant + antiplatelet mechanism. Not supported by clinical trial data. DOACs should generally be held before eptifibatide administration in elective settings.
Pricing updated 2026-04-09
Bleeding is the primary safety concern with eptifibatide, and it should not be minimized. The drug blocks the final step in platelet aggregation. When you combine that with heparin and aspirin (which is standard practice in every clinical trial and real-world protocol), bleeding risk goes up substantially. The most common bleeding site is the femoral artery access point used during catheterization. Vascular access site hematomas are frequent. Major bleeding events reported across trials include gastrointestinal hemorrhage, genitourinary bleeding, and retroperitoneal hemorrhage. Intracranial hemorrhage is rare but has been reported. The risk of any major bleed increases with concurrent anticoagulant and antiplatelet therapy, advanced age, low body weight, and renal impairment. Thrombocytopenia occurs in approximately 1 to 3% of patients receiving eptifibatide. That means the platelet count drops below 100,000/mm3. More concerning is acute profound thrombocytopenia (platelets below 20,000/mm3), which hits about 0.1 to 0.2% of patients. This can appear within hours of the first bolus. Platelet counts must be checked within 6 hours of the initial dose and daily during the infusion. If platelets fall below 100,000, the infusion stops immediately. Hypotension is commonly observed during the infusion. Other reported side effects include nausea, headache, and back pain. Anaphylaxis has been reported rarely. Eptifibatide is contraindicated in patients with active internal bleeding, bleeding diathesis within 30 days, hemorrhagic stroke or any stroke within 30 days, severe uncontrolled hypertension (systolic above 200 mmHg or diastolic above 110 mmHg), major surgery within 6 weeks, or baseline platelet count below 100,000/mm3. It carries FDA Pregnancy Category B; use only if clearly needed. Whether the drug passes into breast milk is unknown. If you notice unusual bruising, blood in urine or stool, persistent oozing from an access site, sudden headache, or dizziness during or after infusion, the care team needs to know immediately. Platelet function recovers within 4 to 8 hours of discontinuation due to the reversible binding, but active bleeding requires immediate management.
Verify Eptifibatide (Integrilin) dosing and safety with a second opinion
FDA-approved pharmaceutical-grade product supplied as a sterile, ready-to-use solution. Administered exclusively in hospital or cath lab settings under continuous physician supervision. Multiple FDA-approved generic manufacturers. No compounding, grey-market supply, or self-administration risk pathway exists.
| Test | When | Target |
|---|---|---|
| Platelet Count (CBC) | Baseline before bolus; within 6 hours of first dose; then daily during infusion | Baseline >100,000/mm³ to initiate; stop if drops below 100,000/mm³ during therapy; urgent action if <20,000/mm³ |
| Hemoglobin / Hematocrit | Baseline; post-procedure; daily during prolonged infusion if clinically indicated | Baseline; flag if Hgb decreases >2 g/dL from baseline during therapy |
| Serum Creatinine / eGFR (CrCl by Cockcroft-Gault) | Pre-treatment (before bolus) | CrCl ≥50 mL/min: standard infusion. CrCl <50 mL/min: reduce to 1 mcg/kg/min. CrCl <10 or dialysis: do not use. |
| Activated Clotting Time (ACT) | During concurrent heparin administration for PCI | ACT 200–300 sec when eptifibatide + UFH co-administered during PCI |
| aPTT or Anti-Xa Level | If low molecular weight heparin (LMWH) is co-administered instead of UFH | aPTT 50–70 sec (if UFH used post-procedure); anti-Xa 0.5–1.0 IU/mL (if LMWH) |
Detect acute profound thrombocytopenia (0.1–0.2% incidence). Mandatory FDA-label requirement. Stop drug immediately if platelet <100,000/mm³.
Detect clinically significant bleeding (access site, GI, retroperitoneal). Hgb drop >2 g/dL warrants bleeding source evaluation.
Determines infusion rate: standard 2 mcg/kg/min (CrCl ≥50) vs reduced 1 mcg/kg/min (CrCl <50). Eptifibatide is not approved for dialysis: use not recommended.
Guides heparin dose adjustment when co-administered. Eptifibatide itself does not prolong ACT significantly but concurrent heparin requires monitoring.
Standard anticoagulation monitoring when transitioning from or co-administering LMWH with eptifibatide in ACS management
Rapid onset of platelet inhibition following IV bolus; >80% GP IIb/IIIa receptor occupancy achieved
Near-complete inhibition of platelet aggregation; therapeutic antiplatelet effect established
Steady-state plasma levels achieved with continuous infusion; sustained platelet inhibition
Platelet function begins to recover as eptifibatide dissociates from GP IIb/IIIa receptors
Near-complete restoration of normal platelet aggregation; bleeding time normalizes
0 to 5 minutes (IV bolus): GP IIb/IIIa blockade starts immediately. The 180 mcg/kg bolus pushes receptor occupancy past 80% within minutes. Plasma concentration peaks at the end of the push. Mild blood pressure drops occasionally show up during rapid administration. 5 to 30 minutes (early procedural window): Platelet aggregation inhibition climbs above 90% at full therapeutic levels. The continuous infusion locks in steady-state receptor occupancy. If you're following the ESPRIT double-bolus protocol, the second 180 mcg/kg at the 10-minute mark fills the inhibition dip that serial aggregometry studies confirmed with single dosing. Access site oozing and nausea are the most commonly noted issues in this window. 1 to 72 hours (infusion phase): Steady-state platelet inhibition holds above 80% throughout the drip. Thrombocytopenia risk peaks in the first 24 hours, so platelet count checks are mandatory. Hemoglobin trending picks up subclinical bleeding. The most common complication during this phase is femoral access site hematoma. GI bleeding runs around 1 to 2%. Patients frequently report back pain from positioning, along with nausea and headache. 4 to 8 hours after stopping: Platelet function starts coming back as eptifibatide dissociates from the receptor. The 2.5-hour half-life means about 97% clearance within 10 hours (roughly 4 half-lives). This recovery speed is the fastest of any GP IIb/IIIa inhibitor. Abciximab takes 12 to 24 hours or more; clopidogrel takes days. No drug-specific adverse effects appear during the offset period. 12 to 24 hours after stopping: Bleeding time and platelet aggregation return to near-normal. Arterial sheath removal is safe once ACT drops below 175 seconds. Patients on radial access can often ambulate the same day. Femoral access cases need ACT confirmation before sheath pull. Renal impairment (CrCl below 50 mL/min) slows the offset, so expect longer monitoring in those patients.
Immediate onset of GP IIb/IIIa blockade following IV bolus. >80% inhibition of ADP-induced platelet aggregation achieved within 5 minutes at 180 mcg/kg dose. Plasma Cmax reached at end of bolus.
No self-report data (hospital-only). Cath lab clinical observation: platelet inhibition confirmed by rapid ACT/LTA measurements in procedural settings.
Near-complete platelet aggregation inhibition (>90% at therapeutic concentrations). Steady-state receptor occupancy maintained by continuous infusion. Clinical trial ACT targets achieved with concurrent heparin.
Clinical: second bolus at 10 min (ESPRIT) fills the receptor occupancy dip confirmed by serial light transmittance aggregometry in catheterization laboratory studies.
Continuous infusion maintains steady-state platelet inhibition >80%. Platelet count surveillance required: thrombocytopenia risk peaks in first 24h. Hemoglobin trending for subclinical bleeding.
Clinical: access site hematomas (femoral approach) most common complication. GI bleeding uncommon but requires monitoring. Patient complaints: back pain (positioning), nausea, headache.
Reversible, competitive binding results in platelet function return to near-normal within 4–8h as eptifibatide dissociates. Half-life of ~2.5h means 97% clearance within ~4 half-lives (~10h).
Clinical: highly valued feature in patients who may require urgent CABG or other surgery. Faster reversal than any other GP IIb/IIIa inhibitor (abciximab: 12–24h+; clopidogrel: days).
Near-complete normalization of bleeding time and platelet aggregation. Safe for arterial sheath removal once ACT normalizes (<175 sec). Renal impairment (CrCl <50) prolongs offset: monitor accordingly.
Clinical: same-day ambulation achievable in radial access cases; femoral access cases require ACT confirmation before sheath pull.
Source: FDA label (NDA 020718); plasma elimination half-life ~2.5 hours in patients with coronary artery disease
Loading the interactive decay curve.
Eptifibatide (Integrilin) received FDA approval in 1998 under NDA 020718. The FDA-approved prescribing information was most recently updated in 2021. The drug is classified as a prescription injectable pharmaceutical product, not a research peptide or dietary supplement. Multiple FDA-approved generic manufacturers now produce eptifibatide injection. The original branded Integrilin product is no longer actively marketed as a branded item in the US; generic eptifibatide has fully replaced it. Hospital billing uses J-code J1327 (eptifibatide injection, 5 mcg). Eptifibatide is administered exclusively in hospital or catheterization laboratory settings under physician supervision. It is not available for outpatient dispensing, compounding pharmacy purchase, or self-administration. Athletes should note that antiplatelet agents are not listed on the WADA Prohibited List, though use would require appropriate medical documentation. This content is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare provider.
Peptide Schedule Research TeamReviewed Apr 20265 Citations
