Inibitore aromatasi non steroideo

A number of investigators have reported on a rather rare syndrome of excess aromatase activity. In boys, it can lead to gynecomastia , and in girls to precocious puberty and gigantomastia . In both sexes, early epiphyseal closure leads to short stature. This condition is due to mutations in the CYP19A1 gene which encodes aromatase. [16] It is inherited in an autosomal dominant fashion. [17] It has been suggested that the pharaoh Akhenaten and other members of his family may have suffered from this disorder, [18] but more recent genetic tests suggest otherwise. [19] It is one of the causes of familial precocious puberty—a condition first described in 1937. [20]

ARQ-197 has been shown to prevent HGF/c-met induced cellular responses in vitro. ARQ-197 possesses antitumor activity; inhibiting proliferation of A549, DBTRG and NCI-H441 cells with IC50 of , , μM. Treatment with ARQ-197 results in a decrease in phosphorylation of the MAPK signaling cascade and prevention of invasion and migration. In addition, ectopic expression of c-Met in NCI-H661, a cell line having no endogenous expression of c-Met, causes it to acquire an invasive phenotype that is also suppressed by ARQ-197. Although the addition of increasing concentrations of ARQ-197 does not significantly affect the K m of ATP, exposure of c-Met to μM ARQ-197 decreased the V max of c-Met by approximately 3-fold. The ability of ARQ-197 to decrease the V max without affecting the Km of ATP confirmed that ARQ-197 inhibits c-Met through a non–ATP-competitive mechanism and may therefore account for its high degree of kinase selectivity. ARQ-197 prevents human recombinant c-Met with a calculated inhibitory constant K i of approximately 355 nM. Although the highest concentration of ATP used is 200 μM, the potency of ARQ-197 against c-Met is not reduced by using concentrations of ATP up to 1 mM. ARQ-197 blocks c-Met phosphorylation and downstream c-Met signaling pathways. ARQ-197 suppresses constitutive and ligand-mediated c-Met autophosphorylation and, by extension, c-Met activity, in turn leading to the inhibition of downstream c-Met effectors. ARQ-197 induction of caspase-dependent apoptosis is increased in c-Met–expressing human cancer cells including HT29, MKN-45, and MDA-MB-231 cells. [1] [2]

To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor. Please refer to this study by its identifier (NCT number): NCT02437318
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Sponsors and Collaborators Novartis Pharmaceuticals Investigators Study Director: Novartis Pharmaceuticals Novartis Pharmaceuticals More Information Go to  Study Description Study Design Arms and Interventions Outcome Measures Eligibility Criteria Contacts and Locations More Information
Responsible Party: Novartis Pharmaceuticals Identifier: NCT02437318     History of Changes Other Study ID Numbers: CBYL719C2301
2015-000340-42 ( EudraCT Number )
First Posted: May 7, 2015    Key Record Dates Last Update Posted: February 5, 2018 Last Verified: February 2018 Individual Participant Data (IPD) Sharing Statement: Plan to Share IPD: Undecided Plan Description: Novartis is committed to sharing with qualified external researchers, access to patient-level data and supporting clinical documents from eligible studies. These requests are reviewed and approved by an independent review panel on the basis of scientific merit. All data provided is anonymized to respect the privacy of patients who have participated in the trial in line with applicable laws and regulations.

Inibitore aromatasi non steroideo

inibitore aromatasi non steroideo

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