1001917-37-8 Usage
Description
3-(1-Methyl-1H-pyrazol-4-yl)-5-oxo-N-(2-pyridinylmethyl)-5H-benzo[4,5]cyclohepta[1,2-b]pyridine-7-methanesulfonamide, also known as MK 8033, is a novel and specific dual ATP competitive c-Met/Ron inhibitor. It is a pharmaceutical compound designed to target and inhibit the activity of c-Met and Ron proteins, which are often dysregulated in various types of cancer. MK 8033's unique structure allows it to bind to the ATP-binding sites of these proteins, thereby preventing their activation and subsequent promotion of cancer cell growth and survival.
Uses
Used in Cancer Treatment:
MK 8033 is used as an anticancer agent for the treatment of various types of cancer. Its dual inhibition of c-Met and Ron proteins modulates several oncological signaling pathways, leading to the suppression of tumor growth, angiogenesis, and metastasis. By targeting these two proteins, MK 8033 has the potential to be effective against a wide range of cancer types, particularly those with high c-Met and Ron activity.
Used in Drug Development and Research:
In addition to its direct application in cancer treatment, MK 8033 is also used as a research tool in the development of new cancer therapies. Its specificity for c-Met and Ron proteins makes it a valuable compound for studying the roles of these proteins in cancer biology and for identifying potential synergistic effects when combined with other targeted therapies or conventional chemotherapeutic drugs.
Used in Pharmaceutical Industry:
MK 8033 is utilized in the pharmaceutical industry for the development of new drugs targeting c-Met and Ron proteins. Its unique dual inhibition mechanism offers a promising approach to cancer treatment, and further research and development efforts are focused on optimizing its efficacy, safety, and delivery methods. The pharmaceutical industry is continuously exploring the potential of MK 8033 and similar compounds to improve cancer treatment options and outcomes for patients.
Check Digit Verification of cas no
The CAS Registry Mumber 1001917-37-8 includes 10 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 7 digits, 1,0,0,1,9,1 and 7 respectively; the second part has 2 digits, 3 and 7 respectively.
Calculate Digit Verification of CAS Registry Number 1001917-37:
(9*1)+(8*0)+(7*0)+(6*1)+(5*9)+(4*1)+(3*7)+(2*3)+(1*7)=98
98 % 10 = 8
So 1001917-37-8 is a valid CAS Registry Number.
1001917-37-8Relevant articles and documents
Discovery of 1-[3-(1-methyl-1H-pyrazol-4-yl)-5-oxo-5H-benzo[4,5] cyclohepta[1,2-b]pyridin-7-yl]-N-(pyridin-2-ylmethyl)methanesulfonamide (MK-8033): A specific c-Met/Ron dual kinase inhibitor with preferential affinity for the activated state of c-Met
Northrup, Alan B.,Katcher, Matthew H.,Altman, Michael D.,Chenard, Melissa,Daniels, Matthew H.,Deshmukh, Sujal V.,Falcone, Danielle,Guerin, David J.,Hatch, Harold,Li, Chaomin,Lu, Wei,Lutterbach, Bart,Allison, Timothy J.,Patel, Sangita B.,Reilly, John F.,Reutershan, Michael,Rickert, Keith W.,Rosenstein, Craig,Soisson, Stephen M.,Szewczak, Alexander A.,Walker, Deborah,Wilson, Kevin,Young, Jonathan R.,Pan, Bo-Sheng,Dinsmore, Christopher J.
, p. 2294 - 2310 (2013/06/04)
This report documents the first example of a specific inhibitor of protein kinases with preferential binding to the activated kinase conformation: 5H-benzo[4,5]cyclohepta[1,2-b]pyridin-5-one 11r (MK-8033), a dual c-Met/Ron inhibitor under investigation as a treatment for cancer. The design of 11r was based on the desire to reduce time-dependent inhibition of CYP3A4 (TDI) by members of this structural class. A novel two-step protocol for the synthesis of benzylic sulfonamides was developed to access 11r and analogues. We provide a rationale for the observed selectivity based on X-ray crystallographic evidence and discuss selectivity trends with additional examples. Importantly, 11r provides full inhibition of tumor growth in a c-Met amplified (GTL-16) subcutaneous tumor xenograft model and may have an advantage over inactive form kinase inhibitors due to equal potency against a panel of oncogenic activating mutations of c-Met in contrast to c-Met inhibitors without preferential binding to the active kinase conformation.