Gastric Cancer|Inhibitors Agonists Modulators Antagonists|HmoBio.com

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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
H8125	Telatinib	332012-40-5	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.
H8086	Apatinib	1218779-75-9	Apatinib (YN968D1) is a multitargeted tyrosine kinase inhibitor (TKI) that inhibits VEGFR-2 (Flk-1/KDR, IC50=1 nM), RET, c-Kit and c-Src (IC50=13, 429 and 530 nM respectively); significantly increases the accumulation of DOX and Rho 123 in cells overexpressing ABCB1 and ABCG2, inhibits cellular phosphorylation of VEGFR-2, c-kit and PDGFRβ, effectively inhibits proliferation, migration and tube formation of HUVECs induced by FBS, and blocks the budding of rat aortic ring; effectively inhibits the growth of several human tumor xenograft models with little toxicity alone and in combination with chemotherapeutic agents.
H7955	Sunitinib	557795-19-4	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.
H7738	BMS 777607	1025720-94-8	BMS 777607 is a potent, selective, orally efficacious inhibitor of Met kinase with IC50 of 3.9 nM, also potently inhibits Ron, Axl, Tyro-3 and Mer (IC50<15 nM), 40-fold selectivity over Lck, VEGFR-2 and TrkA/B; inhibits cell scattering activated by exogenous HGF in c-Met-expressing PC-3 and DU145 prostate cancer cells, suppresses HGF-stimulated cell migration and invasion with IC50 of <0.1 uM; potently blocks HGF-stimulated c-Met autophosphorylation and downstream activation of Akt and ERK at nanomolar level; demonstrates complete tumor stasis in Met-dependent GTL-16 human gastric carcinoma xenograft models.
H7726	DCC-2618	1442472-39-0	DCC-2618 (Ripretinib, DCC2618) is a potent, oral inhibitor of singly and doubly mutated KIT with IC50 of WT (IC50=4 nM), V654A (8 nM), T670I (18 nM), D816H (5 nM), D816V; also inhibits PDGFRα/β, KDR and cFMS, robustly inhibits exon 17, exon 9/13, exon 9/14, and exon 9/17 KIT mutants, as well as exon 11/17 KIT mutants; inhibits wild type and mutant KIT phosphorylation in cancer cells, demonstrates the potential to treat KIT mutant-driven cancers including GIST, systemic mastocytosis, AML, or melanoma.
H7722	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.
H7241	TAS-116	1260533-36-5	TAS-116 is a novel potent, selective, orally available HSP90α/β inhibitor with Ki of 34.7, 21.3, >50,000, and >50,000 nM for HSP90α, HSP90β, GRP94, and TRAP1, respectively; induces cytotoxicity selectively and potently in MM cell lines and patient MM cells, without toxicity in normal PBMNCs; potently targets HSP90 client proteins including C-Raf and MEK1/2; also inhibits upregulation of HSP27 and overcomes 17-AAG resistance mechanisms in MM cells; demonstrates potent antitumor activity and minimal ocular toxicity in preclinical models.
H6896	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.
H6895	Afuresertib	1047644-62-1	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.
H5586	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.

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