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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Puri R N, Hu C J, Bradford H N, Matsueda R, Umeyama H, Colman R W

Thrombosis Research Center and Department of Medicine, Temple University, Philadelphia, PA 19140.

Trans Assoc Am Physicians. 1989;102:13-9.

A synthetic peptide disulfide, Gln-Val-Val-Cys(NpyS)-Gly-NH2 (P1) inhibited thrombin and plasmin-induced platelet aggregation and cleavage of aggregin. P1 did not inhibit platelet aggregation induced by other agonists nor did it inhibit shape change. 2. P1 also inhibited purified platelet calpain II. 3. The correspondence between the molecular structure of P1 and inhibitory sequence of the peptide in domain 2 of high molecular weight kininogen has shed light on the molecular nature of the cellular mechanism underlying thrombin- and plasmin-induced platelet aggregation and the inhibition by P1. 4. P1 may prove to be useful in designing and improving future protocols of thrombolytic therapy to prevent reocclusion. P1 may also have a role in inhibiting thrombin formed during angioplasty and thus preventing restenosis.

一种合成肽二硫键，谷氨酰胺-缬氨酸-缬氨酸-半胱氨酸（NpyS）-甘氨酸-氨基（P1）可抑制凝血酶和纤溶酶诱导的血小板聚集以及聚集素的裂解。P1不抑制其他激动剂诱导的血小板聚集，也不抑制形态变化。2. P1还可抑制纯化的血小板钙蛋白酶II。3. P1的分子结构与高分子量激肽原结构域2中肽的抑制序列之间的对应关系，揭示了凝血酶和纤溶酶诱导血小板聚集以及P1抑制作用背后细胞机制的分子本质。4. P1可能在设计和改进未来的溶栓治疗方案以预防再闭塞方面有用。P1在抑制血管成形术期间形成的凝血酶从而预防再狭窄方面也可能发挥作用。

Puri R N, Hu C J, Bradford H N, Matsueda R, Umeyama H, Colman R W

Thrombosis Research Center and Department of Medicine, Temple University, Philadelphia, PA 19140.

Trans Assoc Am Physicians. 1989;102:13-9.

A synthetic peptide disulfide, Gln-Val-Val-Cys(NpyS)-Gly-NH2 (P1) inhibited thrombin and plasmin-induced platelet aggregation and cleavage of aggregin. P1 did not inhibit platelet aggregation induced by other agonists nor did it inhibit shape change. 2. P1 also inhibited purified platelet calpain II. 3. The correspondence between the molecular structure of P1 and inhibitory sequence of the peptide in domain 2 of high molecular weight kininogen has shed light on the molecular nature of the cellular mechanism underlying thrombin- and plasmin-induced platelet aggregation and the inhibition by P1. 4. P1 may prove to be useful in designing and improving future protocols of thrombolytic therapy to prevent reocclusion. P1 may also have a role in inhibiting thrombin formed during angioplasty and thus preventing restenosis.

一种合成肽二硫键，谷氨酰胺-缬氨酸-缬氨酸-半胱氨酸（NpyS）-甘氨酸-氨基（P1）可抑制凝血酶和纤溶酶诱导的血小板聚集以及聚集素的裂解。P1不抑制其他激动剂诱导的血小板聚集，也不抑制形态变化。2. P1还可抑制纯化的血小板钙蛋白酶II。3. P1的分子结构与高分子量激肽原结构域2中肽的抑制序列之间的对应关系，揭示了凝血酶和纤溶酶诱导血小板聚集以及P1抑制作用背后细胞机制的分子本质。4. P1可能在设计和改进未来的溶栓治疗方案以预防再闭塞方面有用。P1在抑制血管成形术期间形成的凝血酶从而预防再狭窄方面也可能发挥作用。