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K-Ras G12C-IN-3

CAS# 1629268-19-4

K-Ras G12C-IN-3

Catalog No. BCC5540----Order now to get a substantial discount!

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Chemical structure

K-Ras G12C-IN-3

3D structure

Chemical Properties of K-Ras G12C-IN-3

Cas No. 1629268-19-4 SDF Download SDF
PubChem ID 92044410 Appearance Powder
Formula C21H19Cl3N2O3 M.Wt 453.75
Type of Compound N/A Storage Desiccate at -20°C
Solubility DMSO : ≥ 30 mg/mL (66.12 mM)
*"≥" means soluble, but saturation unknown.
Chemical Name 1-[4-[4-chloro-5-(2,5-dichlorophenyl)-2-methoxybenzoyl]piperazin-1-yl]prop-2-en-1-one
SMILES COC1=C(C=C(C(=C1)Cl)C2=C(C=CC(=C2)Cl)Cl)C(=O)N3CCN(CC3)C(=O)C=C
Standard InChIKey RPBHAPLCWWQJAK-UHFFFAOYSA-N
Standard InChI InChI=1S/C21H19Cl3N2O3/c1-3-20(27)25-6-8-26(9-7-25)21(28)16-11-15(18(24)12-19(16)29-2)14-10-13(22)4-5-17(14)23/h3-5,10-12H,1,6-9H2,2H3
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

K-Ras G12C-IN-3 Dilution Calculator

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K-Ras G12C-IN-3 Molarity Calculator

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Preparing Stock Solutions of K-Ras G12C-IN-3

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.2039 mL 11.0193 mL 22.0386 mL 44.0771 mL 55.0964 mL
5 mM 0.4408 mL 2.2039 mL 4.4077 mL 8.8154 mL 11.0193 mL
10 mM 0.2204 mL 1.1019 mL 2.2039 mL 4.4077 mL 5.5096 mL
50 mM 0.0441 mL 0.2204 mL 0.4408 mL 0.8815 mL 1.1019 mL
100 mM 0.022 mL 0.1102 mL 0.2204 mL 0.4408 mL 0.551 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Background on K-Ras G12C-IN-3

K-Ras G12C-IN-3 is a novel and irreversible inhibitor of mutant K-ras G12C. IC50 value: Target: K-ras G12C inhibitor For more information, please see the following patent. Heterocyclic compounds as covalent inhibitors of G12C mutant K-Ras protein useful for treating cancers, and preparation thereof By Ren, Pingda; Liu, Yi; Li, Liansheng; Feng, Jun; Wu, Tao From PCT Int. Appl. (2014), WO 2014152588 A1 20140925.

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References on K-Ras G12C-IN-3

Co-dependency of PKCdelta and K-Ras: inverse association with cytotoxic drug sensitivity in KRAS mutant lung cancer.[Pubmed:28368426]

Oncogene. 2017 Jul 27;36(30):4370-4378.

Recent studies suggest that the presence of a KRAS mutation may be insufficient for defining a clinically homogenous molecular group, as many KRAS mutant tumors lose reliance on K-Ras for survival. Identifying pathways that support K-Ras dependency may define clinically relevant KRAS subgroups and lead to the identification of new drug targets. We have analyzed a panel of 17 KRAS mutant lung cancer cell lines classified as K-Ras-dependent or -independent for co-dependency on protein kinase C delta (PKCdelta). We show that functional dependency on K-Ras and PKCdelta co-segregate, and that dependency correlates with a more epithelial-like phenotype. Furthermore, we show that the pro-apoptotic and pro-tumorigenic functions of PKCdelta also segregate based on K-Ras dependency, as K-Ras-independent cells are more sensitive to topoisomerase inhibitors, and depletion of PKCdelta in this subgroup suppresses apoptosis through increased activation of extracellular signal-regulated kinase (ERK). In contrast, K-Ras-dependent lung cancer cells are largely insensitive to topoisomerase inhibitors, and depletion of PKCdelta can increase apoptosis and decrease activation of ERK in this subgroup. We have previously shown that nuclear translocation of PKCdelta is necessary and sufficient for pro-apoptotic signaling. Our current studies show that K-Ras-dependent cells are refractive to PKCdelta-driven apoptosis. Analysis of this subgroup showed increased PKCdelta expression and an increase in the nuclear:cytoplasmic ratio of PKCdelta. In addition, targeting PKCdelta to the nucleus induces apoptosis in K-Ras-independent, but not K-Ras-dependent non-small-cell lung cancer (NSCLC) cells. Our studies provide tools for identification of the subset of patients with KRAS mutant tumors most amenable to targeting of the K-Ras pathway, and identify PKCdelta as a potential target in this tumor population. These subgroups are likely to be of clinical relevance, as high PKCdelta expression correlates with increased overall survival and a more epithelial tumor phenotype in patients with KRAS mutant lung adenocarcinomas.

siRNA-Encapsulated Hybrid Nanoparticles Target Mutant K-ras and Inhibit Metastatic Tumor Burden in a Mouse Model of Lung Cancer.[Pubmed:28325292]

Mol Ther Nucleic Acids. 2017 Mar 17;6:259-268.

There is an unmet need in the development of an effective therapy for mutant K-ras-expressing non-small-cell lung cancer (NSCLC). Although various small molecules have been evaluated, an effective therapy remains a dream. siRNAs have the potential to downregulate mutant K-ras both at the protein and mRNA levels. However, a safe and effective delivery of siRNAs to tumors remains a limitation to their translational application in the treatment of this highly debilitating disease. Here we developed a novel hybrid nanoparticle carrier for effective delivery of anti-mutant K-ras to NSCLC (AKSLHN). The ability of this treatment modality to regress lung tumors in mouse models was evaluated as a monotherapy or as a combination treatment with erlotinib. Further, the toxicity of this treatment modality to healthy tissues was evaluated, along with its ability to elicit immune/inflammatory reactions. The results suggest that this treatment modality is a promising prospect for the treatment of mutant K-ras-expressing NSCLC without any accompanying toxicity. However, further understanding of the cellular-level interaction between AHSLHN and erlotinib needs to be attained before this promising treatment modality can be brought to the bedside.

No back seat for a progression event-K-RAS as a therapeutic target in CRC.[Pubmed:28314765]

Genes Dev. 2017 Feb 15;31(4):333-335.

KRAS is the most frequently mutated oncogene in human cancer and plays a central, although poorly understood, role in colorectal cancer (CRC) progression. In this issue of Genes & Development, Boutin and colleagues (pp. 370-382) present a new mouse model of CRC in which the expression of oncogenic K-RAS is regulated by doxycycline. Using this model, they demonstrate that continued expression of oncogenic K-RAS is required for the survival of primary and metastatic colon cancers and that oncogenic K-RAS activates TGF-beta signaling to promote tumor invasion and metastasis.

Clinicopathological and prognostic features of surgically resected pathological stage I lung adenocarcinoma harboring epidermal growth factor receptor and K-ras mutation.[Pubmed:28322512]

Thorac Cancer. 2017 May;8(3):229-237.

BACKGROUND: This study aimed to evaluate mutations of the epidermal growth factor receptor (EGFR) and K-ras genes and their clinicopathological and prognostic features in patients with resected pathological stage I adenocarcinoma. METHODS: We examined 224 patients with surgically resected lung adenocarcinoma and analyzed the prognostic and predictive value of these mutations in 162 patients with pathological stage I adenocarcinoma. RESULTS: Mutations of the EGFR and K-ras genes were detected in 100 (44.6%) and 19 (8.5%) of all tumors, and in 81 (50.0%) and 17 (10.5%) of the pathological stage I tumors, respectively. EGFR mutations were significantly associated with female gender, smoking habit (never smoker), and low grade. By contrast, K-ras mutations were significantly associated with male gender, smoking habit (ever smoker), and the presence of mucinous components. No significant differences were observed in recurrence-free or overall survival between the EGFR-mutant, K-ras-mutant, and wild-type groups (five-year recurrence-free survival 77.8% vs. 87.8% vs. 79.5%; five-year overall survival 82.8% vs. 82.4% vs. 79.2%, respectively). Multivariate analysis showed that neither EGFR nor K-ras mutation was an independent prognostic factor. CONCLUSIONS: The present study demonstrated that pathological stage I adenocarcinoma harboring EGFR and K-ras gene mutations have distinct clinicopathological features. The presence of these mutations alone were not prognostic factors in patients with resected pathological stage I adenocarcinoma.

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K-Ras G12C-IN-3 is a novel and irreversible inhibitor of mutant K-ras G12C.

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