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In vitro transcription of capped mRNA with modified nucleotides and Poly(A) tail
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody
A convenient and sensitive way for cell proliferation assay and cytotoxicity assay
Protect the integrity of proteins from multiple proteases and phosphatases for different applications.
Oncrasin 1 is a small molecule antitumor agent with IC50 value of 4.81 μM [1].The activated mutations of Ras genes (K-Ras, N-Ras and H-Ras) play important roles in tumorigenesis and maintenance of malignant phenotypes. The mutations make Ras constitutively be in the activated state with GTP-bound. Among the three Ras genes, the mutations of K-Ras are the most frequently found in tumors and are associated with resistance to radio therapy, chemotherapy and poor prognosis. Thus, mutant K-Ras is important target for antitumor treatment. Oncrasin 1 is a small-molecule compound that found by a synthetic lethality screening. It effectively killed tumor cells with K-Ras mutation but not normal isogenic cells through inducing cell apoptosis. Besides that, Oncrasin 1 caused abnormal aggregation of PKCι of those sensitive cells [1].In a sulforhodamine B (SRB) assay, treatment of Oncrasin 1 at final concentration of 5 μg/ml killed more than 50% of cells. Oncrasin 1 was highly selective against K-Ras mutation, it showed dose-dependent cytotoxicity in T29Kt1 (K-Ras mutant) cells with IC50 value of 4.81 μM. For T29Ht1 (H-Ras mutant) cells and T29 (wild-type Ras) cells, Oncrasin 1 showed no cytotoxicity even at concentration of 33 μM. For the other K-Ras-mutant tumor cells such as A549, H2122 and H460, Oncrasin 1 all showed cytotoxicity with IC50 value of ≤ 3 μM. It was found that induction of apoptosis was a major mechanism of Oncrasin 1 treatment [1]. In mice injected with H460 cells, administration of Oncrasin 1 at dose of 100 mg/kg resulted in significant tumor growth suppression by 75.4%. In addition, the survival time was prolonged by the Oncrasin 1 treatment [1]. Reference:[1] Guo W, Wu S, Liu J, et al. Identification of a small molecule with synthetic lethality for K-ras and protein kinase C iota. Cancer research, 2008, 68(18): 7403-7408.