P-selectin is a cell adhesion molecule. Usually, P-selectin induces prothrombotic and proinflammatory signaling. P-selectin recruits leukocytes that circulate in the blood to the endothelium. And then activates platelets about the growing thrombus. Besides, platelets activate neutrophil integrins and activated platelets are implicated in NETosis through P-selectin. Generally, soluble P-selectin exists in the blood and circulates in normal humans. Most importantly, the level of P-selectin is related to platelet turnover and its activation and function. Meanwhile, coronary artery disease, acute myocardial infarction, and peripheral artery diseases are always accompanied by an increase in P-selectin. So P-selectin is a good marker of blood cancer and cardiovascular disease. Here, we will introduce a humanized IgG4 monoclonal antibody that targets P-selectin.

Inclacumab is a humanized monoclonal antibody targeting P-selectin.

From: McEver RP, et al. J Clin Invest. 1997 Dec 1;100(11 Suppl):S97-103.

Inclacumab is a fully human IgG4 monoclonal antibody that selectively targets P-selectin. In addition, Inclacumab has safe and persistent inhibitory effects on cell adhesion.

Firstly, according to the in vitro experiment results. Inclacumab dose-dependently inhibits thrombin receptor-activating peptide (TRAP)-induced platelet-leukocyte aggregates (PLA) levels. Besides, Inclacumab inhibits P-selectin glycoprotein ligand 1 (PSGL-1) binding with P-selectin. What’s more, Inclacumab blocks the adhesion of PSGL-1 expressing cells to an immobilized P-selectin. Last but not least, Inclacumab reduces TRAP- and ADP-induced PLA levels in cynomolgus monkeys. Besides, the inhibition result is both effective by subcutaneous injection and intravenous injection.

In conclusion, Inclacumab is a humanized monoclonal antibody that selectively targets P-selectin. Beyond that Inclacumab efficiently decreases PLA levels in vivo and in vitro.


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