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Prexasertib (LY2606368) is a selective checkpoint kinase 1 (CHK1) inhibitor (Ki 0.9 nM, IC50<1 nM). Prexasertib causes double-stranded DNA breaks and replication mutations, leading to apoptosis. Prexasertib has antitumor activity.

Prexasertib is an effective and selective Chk1/Chk2 inhibitor. Prexasertib causes Replication Catastrophe and Antitumor Effects through CHK1-Dependent Mechanisms.

Prexasertib Mesylate Hydrate (LY2606368 Mesylate Hydrate) is an ATP-competitive, selective, second-generation cell cycle checkpoint kinase 1 (CHK1) inhibitor (IC50<1 nM, Ki: 0.9 nM). It inhibits CHK2 (IC50: 8 nM) and RSK1 (IC50: 9 nM), induces double-stranded DNA breaks and replication mutations, triggers apoptosis, and exhibits potent anti-tumor effects.

Prexasertib dimesylate (LY2606368 dimesylate) is a highly selective, ATP-competitive, second-generation inhibitor of checkpoint kinase 1 (CHK1), with a K_i of 0.9 nM and an IC_50 of <1 nM, and also effectively inhibits CHK2 (IC_50 = 8 nM) and RSK1 (IC_50 = 9 nM). Its mechanism induces double-stranded DNA breakage and replication catastrophe, leading to apoptosis, and demonstrates potent anti-tumor activity.

LY2606368 HCl is a selective ATP competitive inhibitor of checkpoint kinase 1 (IC50: 1.5nM in SW1990 cells).

Prexasertib lactate is the lactate salt form of Prexasertib and functions as a selective, ATP-competitive second-generation checkpoint kinase 1 (CHK1) inhibitor with a Ki of 0.9 nM and an IC50 of less than 1 nM. It also inhibits CHK2 (IC50 = 8 nM) and RSK1 (IC50 = 9 nM). This compound induces double-strand DNA breaks and replication stress, leading to apoptosis (cell death), and exhibits antitumor activity.

Prexasertib dihydrochloride (LY2606368) is an ATP-competitive CHK1 inhibitor (Ki: 0.9 nmol/L). in the cell-free assay, its IC50 values are 8 nM and 9 nM for CHK2 and RSK, respectively.

Prexasertib is a potent and selective Chk1/Chk2 inhibitor. Prexasertib increases the effectiveness of conventional therapy in B-/T- cell progenitor acute lymphoblastic leukemia. LY2606368 causes replication catastrophe and antitumor effects through CHK1-d