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Request The Product List ofGastric Cancer Gastric Cancer

    Gastric cancer is now arguably one of the most understood malignancies, and real progress is being made towards eradicating this global killer. Much work still needs to be done to define the optimal approach for eradicating the causative agent, namely H. pylori infection.


   The vast majority of malignant tumours of the stomach are adenocarcinomas. Historically gastric adenocarcinomas were subdivided by the Laurén histological classification into intestinal and diffuse subtypes. The intestinal type appears to arise from a background of chronic atrophic gastritis, with the development of intestinal metaplasia and transition through progressively increasing stages of dysplasia to carcinoma. The intestinal type is the predominant histological type in high-risk countries, more common in men, and increases significantly in incidence with age. The diffuse type does not show marked geographic variation, can arise in the absence of atrophic gastritis, is more common in females, and often occurs in younger patients with a positive family history.4–6 These epidemiological differences lead to the notion that the two histological subtypes had distinct aetiologies. There are, however, problems with this concept. Laurén himself was unable to classify a significant number of tumours as being either intestinal or diffuse, and some tumours show features of both histological subtypes.6 It has become apparent over the recent years that gastric adenocarcinoma can also be subdivided according to the anatomical site at which it arises. Tumours can be said to be proximal, arising in the cardia region of the stomach, or distal arising from non-cardia regions. As with the histological subtypes, there are aetiological and epidemiological differences between the two tumour sub-sites. Until recently, adenocarcinoma of the gastric cardia represented a small proportion of gastric cancers as a whole. The global trend of falling gastric cancer incidence therefore reflects non-cardia cancer incidence. The incidence of carcinoma of the gastric cardia actually appears to be rising. Whilst this may be partly due to more accurate reporting, the dramatic fall in the incidence of distal cancers has not been paralleled for cardia cancers. Gastric cardia cancer is now therefore relatively more common accounting for around 50% of cases of gastric cancer in developed countries.

Cat. No. Product Name CAS No. Information
GY02792

Avapritinib

1703793-34-3

Avapritinib (BLU-285) is a potent and highly selective inhibitor of mutant KIT and PDGFRα with IC50 of 0.6, 0.27 and 0.24 nM for KIT del557-558, KIT D816V and PDGFRA D842V, respectively; displays weak inhibition against WT KIT with IC50 of 73 nM, >150-fold more potent on KIT D816V than several important kinase antitargets such as VEGFR2, SRC and FLT3; inhibits other well-characterized disease-driving KIT mutants both in vitro and in vivo in preclinical models, demonstrates marked activity in patients with diseases associated with KIT and PDGFRA (GIST) activation loop mutations.

GY02105

Afuresertib hydrochloride

1047645-82-8

A potent, selective, ATP-competitive pan-AKT inhibitor with biochemical IC50 of 0.08/2/2.6 nM for AKT1/2/3; also inhibits PKA (IC50=1.3 nM) and AKT1 E17K mutant (IC50=0.2 nM), selective over PKC, PKG isoforms and p70S6K; orally bioactive.

GY06438

LX1606

1033805-22-9

LX1606 (Telotristat ethyl) is a potent, small-molecule inhibitor of peripheral serotonin synthesis, acts by inhibiting tryptophan hydroxylase (TPH) with IC50 of 28 nM, demonstrates potential for the treatment of carcinoid syndrome.

GY06437

Telotristat

1033805-28-5

Telotristat (LP-778902) is a potent, small-molecule inhibitor of peripheral serotonin synthesis, acts by inhibiting tryptophan hydroxylase (TPH) with IC50 of 28 nM, demonstrates potential for the treatment of carcinoid syndrome.

GY06431

Telotristat etiprate

1137608-69-5

Telotristat etiprate (LX1606 hippurate) is an orally active, small-molecule inhibitor of peripheral serotonin synthesis, acts by inhibiting tryptophan hydroxylase (TPH) with IC50 of 28 nM, demonstrates potential for the treatment of carcinoid syndrome.

GY01650

AMG-337

1173699-31-4

AMG-337 is a potent and selective inhibitor of MET with biochemical IC50 of 1 nM; inhibits of HGF-mediated MET phosphorylation in PC3 cells; shows desirable preclinical pharmacokinetics, significant inhibition of MET phosphorylation in mice, and robust tumor growth inhibition in a MET-dependent mouse efficacy model.

GY01593

Telatinib

332012-40-5

Telatinib is an orally active, small molecule inhibitor of VEGFR-2 (IC50=6 nM), VEGFR-3 (IC50=4 nM), PDEGFRα (IC50=15 nM) and c-Kit (IC50=1 nM) in biochemical assays.

GY01481

TSU-68

252916-29-3

TSU-68 (Orantinib, SU6668) is a small-molecule, ATP-competitiv inhibitor of angiogenic related RTKs KDR, PDGFRβ, FGFR1; inhibits receptor tyrosine phosphorylation and mitogenesis after stimulation of cells by appropriate ligands; significant growth inhibition of a diverse panel of human tumor xenografts after oral or i.p. administration.

GY01337

Afuresertib

1047644-62-1

Afuresertib is a potent, selective, ATP-competitive pan-AKT inhibitor with biochemical IC50 of 0.08/2/2.6 nM for AKT1/2/3; also inhibits PKA (IC50=1.3 nM) and AKT1 E17K mutant (IC50=0.2 nM), selective over PKC, PKG isoforms and p70S6K; orally bioactive.

GY01211

Sunitinib

557795-19-4

Sunitinib is a multi-targeted RTK inhibitor that targets VEGFR2 (Flk-1) and PDGFRβ with Ki of 8 nM and 9 nM respectively; displays >10-fold higher selectivity over FGFR-1, EGFR, Cdk2, Met, IGFR-1, Abl, and Src; also inhibits phosphorylation of wild-type FLT3, FLT3-ITD, and FLT3-Asp835 with IC50 of 250 nM, 50 nM, and 30 nM; regresses FLT3-ITD tumors in the subcutaneous tumor xenograft model.

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