This product is an unconjugated, non-therapeutic recombinant analog of abciximab, supplied strictly for research use only. It is built around the platelet integrin GPIIb/IIIa (integrin alphaIIb-beta3) target and reproduces the antigen-binding activity of the originator, which is itself a Fab fragment directed against this receptor. It is provided as a research-grade reagent, not the clinical drug, and is not intended for human or veterinary use. Because it is furnished unconjugated, it is well suited to in-vitro binding studies, receptor-occupancy and neutralization assays, competition and blocking experiments, and as a defined reference or control antibody when characterizing anti-GPIIb/IIIa reagents or biosimilar candidates. Researchers developing conjugates, fusion formats, or ADC-style constructs can use it as a starting binder. The material is offered at low endotoxin levels (research grade typically <1 EU/mg, ultra-low <0.5 EU/mg) and in bulk milligram-to-gram quantities to support assay scale-up, in-vitro standardization, and preclinical workflows. Lot-to-lot consistency and defined specificity make it a practical building block for platelet-biology and antithrombotic mechanism research.
GPIIb/IIIa is the platelet integrin alphaIIb-beta3, encoded by ITGA2B (alphaIIb; UniProt P08514) and ITGB3 (beta3). It is the most abundant receptor on the platelet surface and is largely restricted to platelets and their megakaryocyte precursors. In resting platelets the receptor sits in a low-affinity, bent conformation. Platelet activation by agonists such as thrombin, ADP, or collagen drives inside-out signaling that switches the integrin to a high-affinity, extended state capable of binding fibrinogen and von Willebrand factor via RGD and related recognition motifs. Fibrinogen cross-bridging between adjacent platelets mediates aggregation and thrombus growth, while ligand engagement also initiates outside-in signaling that supports spreading, granule secretion, and clot retraction. As the final common pathway of platelet aggregation, GPIIb/IIIa is a key antithrombotic drug target and is defective in Glanzmann thrombasthenia.