INTRODUCTION: Receptor tyrosine kinase inhibitors have become more significant in these days in order to halt the growth of cancers and malignant tumors. There are various cancers, which can be prevented by means of this pathway. The noteworthy point is that, every cancer exhibits diversity and variation in its propagation and growth. Therefore, different molecules face limitation in their application and usage. In order to minimize these limitations, different research studies are continuously performed for the generation of new molecules that can halt the growth and proliferation of perifosine.
CUDC-101: MECHANISMS CUDC-101 has been developed with such a spectrum, since it faces less resistance and limitation on account of its application for the prevention and decrease in tumor size and cancer. CUDC-101 halts the Histone deacetylase and the receptor kinases present in the epidermis (epidermal growth factor receptor (EGFR). The other types of growth factors on which this molecule acts are human epidermal growth factor receptor 2 (HER2) in various tumors. Since the Histone deacetylase inhibition is integrated, the CUDC-101blocks synergistically the key regulators of EGFR and HER2 signaling pathways. During this process, this molecule attenuates various compensatory pathways like AKT, PF-02341066, HER3, etc. that makes possible for the cancer cells to come out from the effects produced by the conventional EGFR and HER2 inhibitors. CUDC- 101: ADVANTAGES: CUDC-101 has potential to show the effective anti-proliferative and proapoptotic activities against various implanted tumor cells and cancers that have been cultured in various experiments. These tumors cells are found resistant and sensitive against various approved single targeted molecules. RESEARCH STUDIES: The research studies on CUDC-101 showed that it has significant power for improving dramatically the diversity of various tumors that cannot be controlled by means of various other molecules. In addition to that, they use to provide a framework in order to create the individual tiny molecules that can block simultaneously various biochemically different oncogenic targets [1]. CUDC-101 – INHIBITION OF EGFR, HER2, AND HDACIt has been found by means of various research studies that CUDC-101 can block the effectiveness of EGFR and Her3 kinase along with the HDAC enzymes activities. All of these actions performed by this molecule possess greater potency. It means that these actions can be performed by this molecule at a very low concentration, i.e. up to 2.4 nmol per liter. In addition to the blockage of above molecules and pathways; CDUC-101 can block or antagonize the actions of class I and II HDAC molecules. It should be remembered that CDUC -101 can also block the effectiveness of erlotinib-resistant EGFR mutant T790M; however, these effects remain incomplete [2 and 3].
It has now established that CDUC- 101 acts synergistically in order to halt the cancer growth with respect of its combined HDAC inhibition and RTK inhibitory activities. These findings have now been confirmed by means of various experiments and research studies [4]. CUDC-101 – FOR BREAST CANCER CUDC-101 can block the development and growth of various breast cancers, like those which are insensitive to lapatinib, and which are triple negative (estrogen, progesterone and HER2 negative). CUDC-101 – FOR LUNG CANCER CUDC-101 can block or inhibit the proliferation and growth of lung cancer lines which could not be eradicated by means of erlotinib. This molecule can even suppress the growth of lung cancers which possess H1975 having EGFR-T790M mutations. CUDC-101 - CONCLUSION CUDC-101 is a potential molecule and it can be used for various cancers of the body. Still research is going on in order to find new ways and its magnificent properties which can be used for the cancers in human body. This molecule could be a brilliant addition in the lines which could be used to provide a new life to human being. REFERENCES: 1. Cancer therapeutics. Cancer Res; 70(9); 3647–56. ©2010 AACR. 2. Sharma SV, Bell DW, Settleman J, Haber DA. Epidermal growth factor receptor mutations in lung cancer. Nat Rev Cancer 2007;7:169–81. 3. Pao W, Miller VA, Politi KA, et al. Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain. PLoS Med 2005;2:225–35. 4. Chou TC, Talalay P. Quantitative analysis of dose-effect relationships: the combined effects of multiple drugs or enzyme inhibitors. Adv Enzyme Regul 1984;22:27–55.
CUDC-101: MECHANISMS CUDC-101 has been developed with such a spectrum, since it faces less resistance and limitation on account of its application for the prevention and decrease in tumor size and cancer. CUDC-101 halts the Histone deacetylase and the receptor kinases present in the epidermis (epidermal growth factor receptor (EGFR). The other types of growth factors on which this molecule acts are human epidermal growth factor receptor 2 (HER2) in various tumors. Since the Histone deacetylase inhibition is integrated, the CUDC-101blocks synergistically the key regulators of EGFR and HER2 signaling pathways. During this process, this molecule attenuates various compensatory pathways like AKT, PF-02341066, HER3, etc. that makes possible for the cancer cells to come out from the effects produced by the conventional EGFR and HER2 inhibitors. CUDC- 101: ADVANTAGES: CUDC-101 has potential to show the effective anti-proliferative and proapoptotic activities against various implanted tumor cells and cancers that have been cultured in various experiments. These tumors cells are found resistant and sensitive against various approved single targeted molecules. RESEARCH STUDIES: The research studies on CUDC-101 showed that it has significant power for improving dramatically the diversity of various tumors that cannot be controlled by means of various other molecules. In addition to that, they use to provide a framework in order to create the individual tiny molecules that can block simultaneously various biochemically different oncogenic targets [1]. CUDC-101 – INHIBITION OF EGFR, HER2, AND HDACIt has been found by means of various research studies that CUDC-101 can block the effectiveness of EGFR and Her3 kinase along with the HDAC enzymes activities. All of these actions performed by this molecule possess greater potency. It means that these actions can be performed by this molecule at a very low concentration, i.e. up to 2.4 nmol per liter. In addition to the blockage of above molecules and pathways; CDUC-101 can block or antagonize the actions of class I and II HDAC molecules. It should be remembered that CDUC -101 can also block the effectiveness of erlotinib-resistant EGFR mutant T790M; however, these effects remain incomplete [2 and 3].
CUDC-101– SYNERGISTIC EFFECTS
It has now established that CDUC- 101 acts synergistically in order to halt the cancer growth with respect of its combined HDAC inhibition and RTK inhibitory activities. These findings have now been confirmed by means of various experiments and research studies [4]. CUDC-101 – FOR BREAST CANCER CUDC-101 can block the development and growth of various breast cancers, like those which are insensitive to lapatinib, and which are triple negative (estrogen, progesterone and HER2 negative). CUDC-101 – FOR LUNG CANCER CUDC-101 can block or inhibit the proliferation and growth of lung cancer lines which could not be eradicated by means of erlotinib. This molecule can even suppress the growth of lung cancers which possess H1975 having EGFR-T790M mutations. CUDC-101 - CONCLUSION CUDC-101 is a potential molecule and it can be used for various cancers of the body. Still research is going on in order to find new ways and its magnificent properties which can be used for the cancers in human body. This molecule could be a brilliant addition in the lines which could be used to provide a new life to human being. REFERENCES: 1. Cancer therapeutics. Cancer Res; 70(9); 3647–56. ©2010 AACR. 2. Sharma SV, Bell DW, Settleman J, Haber DA. Epidermal growth factor receptor mutations in lung cancer. Nat Rev Cancer 2007;7:169–81. 3. Pao W, Miller VA, Politi KA, et al. Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain. PLoS Med 2005;2:225–35. 4. Chou TC, Talalay P. Quantitative analysis of dose-effect relationships: the combined effects of multiple drugs or enzyme inhibitors. Adv Enzyme Regul 1984;22:27–55.
SHARE
