86811-36-1

86811-36-1 structure

Name: PT-262
Chemical Name: PT-262
CAS Number: 86811-36-1
Molecular Formula: C₁₄H₁₃ClN₂O₂
Molecular Weight: 276.72
Catalog: Signaling Pathways Apoptosis Apoptosis
Create Date: 2023-04-04 13:19:03
Modify Date: 2024-02-03 23:49:54
PT-262 is a potent ROCK inhibitor with an IC50 value of around 5 μM. PT-262 induces the loss of mitochondrial membrane potential and elevates the caspase-3 activation and apoptosis. PT-262 inhibits the ERK and CDC2 phosphorylation via a p53-independent pathway. PT-262 blocks cytoskeleton function and cell migration. PT-262 has anti-cancer activity[1][2].

Name	PT-262

Description	PT-262 is a potent ROCK inhibitor with an IC50 value of around 5 μM. PT-262 induces the loss of mitochondrial membrane potential and elevates the caspase-3 activation and apoptosis. PT-262 inhibits the ERK and CDC2 phosphorylation via a p53-independent pathway. PT-262 blocks cytoskeleton function and cell migration. PT-262 has anti-cancer activity[1][2].
Related Catalog	Signaling Pathways >> Apoptosis >> Apoptosis Research Areas >> Cancer Signaling Pathways >> Cell Cycle/DNA Damage >> ROCK Signaling Pathways >> Cell Cycle/DNA Damage >> CDK Signaling Pathways >> MAPK/ERK Pathway >> ERK Signaling Pathways >> Stem Cell/Wnt >> ROCK Signaling Pathways >> TGF-beta/Smad >> ROCK Signaling Pathways >> Stem Cell/Wnt >> ERK
Target	ROCK:5 μM (IC50) ERK CDK2
In Vitro	PT-262 (5-40 μM; 24 h) induces cytotoxicity and proliferation inhibition in human lung cancer cells[1]. PT-262 (2-20 μM; 4-24 h) induces caspase-3 activation, mitochondrial dysfunction and apoptosis in lung cancer cells[1]. PT-262 (10-20 μM; 24 h) induces the accumulation of G2/M phases in both the p53-wild type and p53-null lung cancer cells, and inhibits the phosphorylation of CDC2 proteins[1]. PT-262 (0-10 μM; 24 h) represses ERK phosphorylation in lung cancer cells[1]. PT-262 (2 μM; 24 h) induces the cytoskeleton alteration and cell elongation in lung carcinoma A549 cells[2]. PT-262 (2-10 μM; 6 h) significantly blocks the cell migration in a concentration-dependent manner[2]. Cell Viability Assay[1] Cell Line: A549 cells Concentration: 5-40 μM Incubation Time: 24 h Result: Reduced the cell viability via a concentration-dependent manner in A549 cells. The IC50 value toward human normal lung fibroblast was >20 μM. Apoptosis Analysis[1] Cell Line: A549 cells Concentration: 2-20 μM Incubation Time: 4-24 h Result: The apoptotic cells were increased after treatment at 10 μM for 8-24 h. The active forms of caspase-3 (12 and 17 kD) were induced following treatment with 2-20 μM for 24 h. Cell Cycle Analysis[1] Cell Line: A549 and H1299 cells Concentration: 10-20 μM Incubation Time: 24 h Result: Significantly decreased the G1 fractions while increased the G2/M fractions in both A549 and H1299 cells with 10 μM for 24 h. Decreased the protein levels of cyclin B1 and phospho-CDC2 at Thr14, Tyr15, and Thr161 via a concentration-dependent manner in A549 cells. Western Blot Analysis[1] Cell Line: A549 cells Concentration: 0-10 μM Incubation Time: 24 h Result: Significantly inhibited the phosphorylation of ERK.
References	[1]. Tzu-Sheng Hsu, et al. 7-Chloro-6-piperidin-1-yl-quinoline-5,8-dione (PT-262), a novel synthetic compound induces lung carcinoma cell death associated with inhibiting ERK and CDC2 phosphorylation via a p53-independent pathway. Cancer Chemother Pharmacol. 2008 Oct;62(5):799-808. [2]. Chih-Chien Tsai, et al. 7-Chloro-6-piperidin-1-yl-quinoline-5,8-dione (PT-262), a novel ROCK inhibitor blocks cytoskeleton function and cell migration. Biochem Pharmacol. 2011 Apr 1;81(7):856-65.

Molecular Formula	C₁₄H₁₃ClN₂O₂
Molecular Weight	276.72

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