Cerdulatinibhydrochloride(PRT062070)是一种选择性，具有口服活性和可逆的ATP竞争性的SYK和JAK的双重抑制剂，抑制SYK和Tyk2、JAK1、2、3的IC50值分别为32nM、0.5nM、12nM、6nM和8nM。Cerdulatinibhydrochloride可用于研究自身免疫性疾病和B细胞恶性肿瘤。
货号:ajcx30364
CAS:1369761-01-2
分子式:C20H28ClN7O3S
分子量：482
溶解度:N/A
纯度：98%
存储：Store at -20°C
库存： 现货

Background:

Cerdulatinib hydrochloride (PRT062070) is a selective, oral active and reversible ATP-competitive inhibitor of dual SYK and JAK, with IC50s of 32 nM, 0.5 nM, 12 nM, 6 nM and 8 nM for SYK and Tyk2, JAK1, 2, 3, respectively. Cerdulatinib hydrochloride could be used to research autoimmune disease and B-cell malignancies[1][2].

Cerdulatinib (0.03-4 μM) inhibits ERK Y204 phosphorylation with an IC50 of 0.5 μM and reduces the ability to upregulate cellsurface expression of the early activation marker CD69 with an IC50 of 0.11 μM in B cells in human whole blood[1].Cerdulatinib (0.015-2 μM) inhibits FcεRI-mediated basophil degranulation with an IC50 of 0.12 μM[1].Cerdulatinib (0.5-4 μM) exhibits differential potency against cytokine JAK/STAT signaling pathways[1].Cerdulatinib (0-15 μM; 72 hours) results in viability effects similar to that of the combines SYK plus JAK-selective inhibition[1].Cerdulatinib (1-3 μM; 48 hours) induces apoptosis in BCR-signaling competent non-Hodgkin lymphoma (NHL) cell lines[1]. Cell Viability Assay[1] Cell Line: SU-DHL4; SU-DHL6; Ramosand and Daudi cells

Cerdulatinib (0.5-5 mg/kg; twice daily p.o. for 2 weeks) elicits dose-dependent efficacy in the rat collagen-induced arthritis (CIA) model[1].Cerdulatinib ( mg/kg; twice daily p.o. for 5 days) blocks BCR-induced B-cell activation and splenomegaly in mice[1]. Animal Model: Female Lewis rats (7-8 weeks old; 159-187 g) are immunized[1]

[1]. Coffey G, et al. The novel kinase inhibitor PRT062070 (Cerdulatinib) demonstrates efficacy in models of autoimmunity and B-cell cancer. J Pharmacol Exp Ther. 2014 Dec; 351(3): 538-48. [2]. Ishikawa C, et, al. Anti-adult T?cell leukemia/lymphoma activity of cerdulatinib, a dual SYK/JAK kinase inhibitor. Int J Oncol. 2018 Oct; 53(4): 1681-1690.