Hot Selling! ! Antineoplastic High Purity Crizotinib 99.5% CAS 877399-52-5

Quick Details

• CAS No.: 877399-52-5
• Other Names: Crizotinib
• MF: C21H22Cl2FN5O
• EINECS No.: 877399-52-5
• Place of Origin: Shanghai, China (Mainland)
• Type: Antineoplastic Agents
• Grade Standard: Medicine Grade
• Usage: Animal Pharmaceuticals
• Brand Name: TwoChem
• Purity: 99.7%

• Crizotinib

  is an anti-cancer drug acting as an ALK (anaplastic lymphoma kinase) and ROS1 (c-ros oncogene 1) inhibitor, approved for treatment of some non-small cell lung carcinoma (NSCLC) in the US and some other countries, and undergoing clinical trials testing its safety and efficacy in anaplastic large cell lymphoma, neuroblastoma, and other advanced solid tumors in both adults and children.
   

  Description	Crizotinib is a potent inhibitor of c-Met and ALK with IC50 of 11 nM and 24 nM in cell-based assays, respectively.
  IC50 & Target	IC50: 11 nM (c-Met), 24 nM (ALK)
  In Vitro	PF-2341066 displays similar potency against c-Met phosphorylation in mIMCD3 mouse or MDCK canine epithelial cells with IC50 of 5 nM and 20 nM, respectivly. PF-2341066 shows improved or similar activity against NIH3T3 cells engineered to express c-Met ATP-binding site mutants V1092I or H1094R or the P-loop mutant M1250T with IC50 of 19 nM, 2 nM and 15 nM, respectively, compared with NIH3T3 cells expressing wild-type receptor with IC50 of 13 nM. In contrast, a marked shift in potency of PF-2341066 is observed against cells engineered to express c-Met activation loop mutants Y1230C and Y1235D with IC50 of 127 nM and 92 nM, respectively, compared with wild-type receptor. PF-2341066 also potently prevents the phosphorylation of c-Met in NCI-H69 and HOP92 cells, with IC50 of 13 nM and 16 nM, respectively, which express the endogenous c-Met variants R988C and T1010I, respectively[1]. PF-2341066 also potently inhibits NPM-ALK phosphorylation in Karpas299 or SU-DHL-1 ALCL cells with an IC50 of 24 nM. PF-2341066 potently prevents cell proliferation, which is associated with G(1)-S-phase cell cycle arrest and induction of apoptosis in ALK-positive ALCL cells with IC50 of 30 nM, but not ALK-negative lymphoma cells[2]. Besides, PF-2341066 prevents osteosarcoma behavior associated with primary tumor growth (i.e., proliferation and survival) as well as metastasis[3].
  In Vivo	PF-2341066 reveals the ability to cause marked regression of large established tumors (> 600 mm3) in both the 50 mg/kg/day and 75 mg/kg/day treatment cohorts, with a 60% decrease in mean tumor volume over the 43-day administration schedule in the GTL-16 model. In an another study, PF-2341066 displays the ability to completely inhibits GTL-16 tumor growth for >3 months, with only 1 of 12 mice exhibiting a significant increase in tumor growth over the 3-month treatment schedule at 50 mg/kg/day. A significant dose-dependent reduction of CD31-positive endothelial cells is observed at 12.5 mg/kg/day, 25 mg/kg/day, and 50 mg/kg/day in GTL-16 tumors, indicating that inhibition of MVD shows a dose-dependent correlation to antitumor efficacy. PF-2341066 displays a significant dose-dependent reduction of human VEGFA and IL-8 plasma levels in both the GTL-16 and U87MG models. Marked inhibition of phosphorylated c-Met, Akt, Erk, PLCλ1, and STAT5 levels is observed in GTL-16 tumors following p.o. administration of PF-2341066[1]. PF-2341066 prevents osteosarcoma behavior associated with primary tumor growth as well as metastasis. In nude mice treated with PF-2341066 via oral gavage, the growth and associated osteolysis and extracortical bone matrix formation of osteosarcoma xenografts are prevented by PF-2341066[3]. Treatment of c-MET-amplified GTL-16 xenografts with 50 mg/kg PF-2341066 elicits tumor regression that is associated with a slow reduction in 18F-FDG uptake and decreases expression of the glucose transporter 1, GLUT-1[4].
  Clinical Trial	NCT Number Sponsor Condition Start Date Phase NCT02034981 UNICANCER|National Cancer Institute, France|Fondation ARC|Pfizer Hematologic Cancers|Solid Tumors|Metastatic Cancer August 2013 Phase 2 NCT02223819 Columbia University|Pfizer Uveal Melanoma March 2015 Phase 2 NCT02499614 Fondazione Ricerca Traslazionale Carcinoma, Non-Small-Cell Lung December 2014 Phase 2 NCT01945021 Pfizer|OxOnc Development LP Non Small Cell Lung Cancer|ROS1 Proto Oncogene|Crizotinib September 2013 Phase 2 NCT02183870 University of Cologne|Spanish Lung Cancer Group|Pfizer Lung Cancer|Adenocarcinoma|NSCLC May 2014 Phase 2

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Quick Details

• CAS No.: 877399-52-5
• Other Names: Crizotinib
• MF: C21H22Cl2FN5O
• EINECS No.: 877399-52-5
• Place of Origin: Shanghai, China (Mainland)
• Type: Antineoplastic Agents
• Grade Standard: Medicine Grade
• Usage: Animal Pharmaceuticals
• Brand Name: TwoChem
• Purity: 99.7%

• Crizotinib

  is an anti-cancer drug acting as an ALK (anaplastic lymphoma kinase) and ROS1 (c-ros oncogene 1) inhibitor, approved for treatment of some non-small cell lung carcinoma (NSCLC) in the US and some other countries, and undergoing clinical trials testing its safety and efficacy in anaplastic large cell lymphoma, neuroblastoma, and other advanced solid tumors in both adults and children.
   

  Description	Crizotinib is a potent inhibitor of c-Met and ALK with IC50 of 11 nM and 24 nM in cell-based assays, respectively.
  IC50 & Target	IC50: 11 nM (c-Met), 24 nM (ALK)
  In Vitro	PF-2341066 displays similar potency against c-Met phosphorylation in mIMCD3 mouse or MDCK canine epithelial cells with IC50 of 5 nM and 20 nM, respectivly. PF-2341066 shows improved or similar activity against NIH3T3 cells engineered to express c-Met ATP-binding site mutants V1092I or H1094R or the P-loop mutant M1250T with IC50 of 19 nM, 2 nM and 15 nM, respectively, compared with NIH3T3 cells expressing wild-type receptor with IC50 of 13 nM. In contrast, a marked shift in potency of PF-2341066 is observed against cells engineered to express c-Met activation loop mutants Y1230C and Y1235D with IC50 of 127 nM and 92 nM, respectively, compared with wild-type receptor. PF-2341066 also potently prevents the phosphorylation of c-Met in NCI-H69 and HOP92 cells, with IC50 of 13 nM and 16 nM, respectively, which express the endogenous c-Met variants R988C and T1010I, respectively[1]. PF-2341066 also potently inhibits NPM-ALK phosphorylation in Karpas299 or SU-DHL-1 ALCL cells with an IC50 of 24 nM. PF-2341066 potently prevents cell proliferation, which is associated with G(1)-S-phase cell cycle arrest and induction of apoptosis in ALK-positive ALCL cells with IC50 of 30 nM, but not ALK-negative lymphoma cells[2]. Besides, PF-2341066 prevents osteosarcoma behavior associated with primary tumor growth (i.e., proliferation and survival) as well as metastasis[3].
  In Vivo	PF-2341066 reveals the ability to cause marked regression of large established tumors (> 600 mm3) in both the 50 mg/kg/day and 75 mg/kg/day treatment cohorts, with a 60% decrease in mean tumor volume over the 43-day administration schedule in the GTL-16 model. In an another study, PF-2341066 displays the ability to completely inhibits GTL-16 tumor growth for >3 months, with only 1 of 12 mice exhibiting a significant increase in tumor growth over the 3-month treatment schedule at 50 mg/kg/day. A significant dose-dependent reduction of CD31-positive endothelial cells is observed at 12.5 mg/kg/day, 25 mg/kg/day, and 50 mg/kg/day in GTL-16 tumors, indicating that inhibition of MVD shows a dose-dependent correlation to antitumor efficacy. PF-2341066 displays a significant dose-dependent reduction of human VEGFA and IL-8 plasma levels in both the GTL-16 and U87MG models. Marked inhibition of phosphorylated c-Met, Akt, Erk, PLCλ1, and STAT5 levels is observed in GTL-16 tumors following p.o. administration of PF-2341066[1]. PF-2341066 prevents osteosarcoma behavior associated with primary tumor growth as well as metastasis. In nude mice treated with PF-2341066 via oral gavage, the growth and associated osteolysis and extracortical bone matrix formation of osteosarcoma xenografts are prevented by PF-2341066[3]. Treatment of c-MET-amplified GTL-16 xenografts with 50 mg/kg PF-2341066 elicits tumor regression that is associated with a slow reduction in 18F-FDG uptake and decreases expression of the glucose transporter 1, GLUT-1[4].
  Clinical Trial	NCT Number Sponsor Condition Start Date Phase NCT02034981 UNICANCER|National Cancer Institute, France|Fondation ARC|Pfizer Hematologic Cancers|Solid Tumors|Metastatic Cancer August 2013 Phase 2 NCT02223819 Columbia University|Pfizer Uveal Melanoma March 2015 Phase 2 NCT02499614 Fondazione Ricerca Traslazionale Carcinoma, Non-Small-Cell Lung December 2014 Phase 2 NCT01945021 Pfizer|OxOnc Development LP Non Small Cell Lung Cancer|ROS1 Proto Oncogene|Crizotinib September 2013 Phase 2 NCT02183870 University of Cologne|Spanish Lung Cancer Group|Pfizer Lung Cancer|Adenocarcinoma|NSCLC May 2014 Phase 2

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