EPI-001, a compound active against castration-resistant prostate cancer, targets transactivation unit 5 of the androgen receptor Castration-resistant prostate cancer is the lethal condition suffered by prostate cancer patients that become refractory to androgen deprivation therapy. EPI-001 is a recently identified compound active against this condition that modulates the activity of the androgen receptor, a nuclear receptor that is essential for disease progression. The mechanism by which this compound exerts its inhibitory activity is however not yet fully understood. Here we show, by using high resolution solution nuclear magnetic resonance spectroscopy, that EPI-001 selectively interacts with a partially folded region of the transactivation domain of the androgen receptor, known
with imaging and/or proteinuria evidence of renal dysfunction, the NWB population again had different eGFR when calculated using CKD-EPI, CKD-EPI and CKD-EPI (<.001). Fifty-eight percent of NWB individuals with evidence of renal dysfunction on imaging or urinalysis were reclassified into a lower eGFR category when using eGFR relative to eGFR. eGFR equations containing serum creatinine, cystatin C, or both
, including EPI-001 (EPI), have the promising ability to block constitutively active splice variants, which represent a major resistance mechanism in CRPC. Autophagy is a conserved lysosomal degradation pathway that acts as survival mechanism in cells exposed to anticancer treatments. We hypothesized, that promising NTD-AR treatment may upregulate autophagy and that a combination of NTD-AR and autophagy
mechanisms include amplification, point mutations, expression of constitutively active splice variants, and altered intratumoral androgen biosynthesis. AR-independent resistance mechanisms include glucocorticoid receptor activation, immune-mediated resistance, and neuroendocrine differentiation. The development of novel agents, such as seviteronel, apalutamide, and EPI-001/EPI-506, as well
interactions. However, due to the intrinsically disordered structure of the domain, its potential as a candidate for therapeutic intervention has been dismissed in the past. The recent emergence of the small molecule EPI-001 has provided evidence that AR-NTD can be targeted therapeutically, independent of the LBD. Targeting of AR-NTD has the potential to disrupt multiple intermolecular interactions between
domain inhibitors (EPI-001), selective AR downregulators or SARDs (AZD-3514), and agents that inhibit both androgen synthesis and receptor binding (TOK-001/galeterone). Promising immunotherapeutic agents include poxvirus vaccines and CTLA-4 inhibitor (ipilimumab). Biologic agents targeting the molecular drivers of disease are also being investigated as single agents, including cabozantinib (Met
Ralaniten, Ralaniten acetate, and EPI-001.BPA substitutes[edit]See also: BisphenolConcerns about the health effects of BPA have led some manufacturers replacing it with other bisphenols, such as bisphenol S and bisphenol F. These are produced in a similar manner to BPA, by replacing acetone with other ketones, which undergo analogous condensation reactions.[7] Thus, in bisphenol F, the F signifies
Groups and Cohorts Outcome Measures Eligibility Criteria Contacts and Locations More Information Responsible Party: Crucell Holland BV ClinicalTrials.gov Identifier: NCT01839760 Other Study ID Numbers: FLU-EPI-001 First Posted: April 25, 2013 Key Record Dates Last Update Posted
of Anogenital Human Papillomavirus Infection in Liuzhou, China: An Observational Cohort Study. Clin Infect Dis. 2020 Jan 1;70(1):82-89. doi: 10.1093/cid/ciz168. Responsible Party: Jun Zhang, professor, Xiamen University ClinicalTrials.gov Identifier: NCT02188004 Other Study ID Numbers: HPV-EPI-001 First Posted