Momic Tatjana, Katzhendler Jehoshua, Shai Ela, Noy Efrat, Senderowitz Hanoch, Eble Johannes A, Marcinkiewicz Cezary, Varon David, Lazarovici Philip
School of Pharmacy Institute for Drug Research, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel.
Department of Hematology, Coagulation Unit, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.
Drug Des Devel Ther. 2015 Jan 5;9:291-304. doi: 10.2147/DDDT.S72844. eCollection 2015.
Linear peptides containing the sequence WKTSRTSHY were used as lead compounds to synthesize a novel peptidomimetic antagonist of α2β1 integrin, with platelet aggregation-inhibiting activity, named Vipegitide. Vipegitide is a 13-amino acid, folded peptidomimetic molecule, containing two α-aminoisobutyric acid residues at positions 6 and 8 and not stable in human serum. Substitution of glycine and tryptophan residues at positions 1 and 2, respectively, with a unit of two polyethylene glycol (PEG) molecules yielded peptidomimetic Vipegitide-PEG2, stable in human serum for over 3 hours. Vipegitide and Vipegitide-PEG2 showed high potency (7×10(-10) M and 1.5×10(-10) M, respectively) and intermediate efficacy (40% and 35%, respectively) as well as selectivity toward α2 integrin in inhibition of adhesion of α1/α2 integrin overexpressing cells toward respective collagens. Interaction of both peptidomimetics with extracellular active domain of α2 integrin was confirmed in cell-free binding assay with recombinant α2 A-domain. Integrin α2β1 receptor is found on the platelet membrane and triggers collagen-induced platelet aggregation. Vipegitide and Vipegitide-PEG2 inhibited α2β1 integrin-mediated adhesion of human and murine platelets under the flow condition, by 50%. They efficiently blocked adenosine diphosphate- and collagen I-induced platelet aggregation in platelet rich plasma and whole human blood. Higher potency of Vipegitide than Vipegitide-PEG2 is consistent with results of computer modeling of the molecules in water. These peptidomimetic molecules were acutely tolerated in mice upon intravenous bolus injection of 50 mg/kg. These results underline the potency of Vipegitide and Vipegitide-PEG2 molecules as platelet aggregation-inhibiting drug lead compounds in antithrombotic therapy.
含有序列WKTSRTSHY的线性肽被用作先导化合物,以合成一种新型的α2β1整合素拟肽拮抗剂,其具有血小板聚集抑制活性,名为Vipegitide。Vipegitide是一种由13个氨基酸组成的折叠拟肽分子,在第6位和第8位含有两个α-氨基异丁酸残基,在人血清中不稳定。分别用两个聚乙二醇(PEG)分子单元取代第1位和第2位的甘氨酸和色氨酸残基,得到在人血清中稳定超过3小时的拟肽Vipegitide-PEG2。Vipegitide和Vipegitide-PEG2在抑制α1/α2整合素过表达细胞与各自胶原蛋白的黏附方面,对α2整合素显示出高效力(分别为7×10(-10) M和1.5×10(-10) M)和中等功效(分别为40%和35%)以及选择性。在与重组α2 A结构域的无细胞结合试验中证实了这两种拟肽与α2整合素细胞外活性结构域的相互作用。整合素α2β1受体存在于血小板膜上,并触发胶原蛋白诱导的血小板聚集。Vipegitide和Vipegitide-PEG2在流动条件下抑制人和小鼠血小板的α2β1整合素介导的黏附达50%。它们有效阻断富含血小板血浆和全血中腺苷二磷酸和I型胶原蛋白诱导的血小板聚集。Vipegitide比Vipegitide-PEG2具有更高的效力,这与分子在水中的计算机模拟结果一致。这些拟肽分子在小鼠静脉推注50 mg/kg时具有急性耐受性。这些结果强调了Vipegitide和Vipegitide-PEG2分子作为抗血栓治疗中血小板聚集抑制药物先导化合物所具有的效力。