España
De estas 2 últimas, nivel de institucionales a 30/06 de DYAX = 99% y de ZSPH = 76%.
Otra que se quiere adquirir, DEPO, en 102% (bueno, son esas cosas raras que pasan cuando hay datos a 30/06 y 30/09 juntos...pero vaya, que cerca del 100% a 30/06)
Preclinical Studies Find That Tarloxotinib May Overcome Resistance to EGFR Tyrosine Kinase Inhibitors
Otro pasito en la buena direccion ... todavia no han reportado un solo estudio con resultados negativos en 4 años que llevo siguiendo esta farma. Pero esto es un preclinico, impacto en el precio ... supuestamente cero patatero.
SOUTH SAN FRANCISCO, CA -- (Marketwired) -- 11/06/15 -- Threshold Pharmaceuticals, Inc. (NASDAQ: THLD) today announced new preclinical data demonstrating that tarloxotinib bromide*, or tarloxotinib, may overcome resistance to first- and second- and third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs). The data will be reported today in two scientific posters (Abstracts A66 and A67) at the AACR-NCI-EORTC Molecular Targets and Cancer Therapeutics Meeting being held November 5-9, 2015, Boston. Tarloxotinib is Threshold's proprietary hypoxia-activated prodrug of an irreversible EGFR TKI exclusively licensed from the University of Auckland, New Zealand.
The research to be reported at the meeting focuses on preclinical models of EGFR-dependent cancers including non-small cell lung cancer (NSCLC) and squamous cell carcinomas of the head and neck (SCCHN) or skin (SCCS). These types of cancers are currently treated with drugs that block the activity of EGFR to interfere with tumor cell growth, but most tumors ultimately become resistant to therapy, and some do not respond at all.
Scientists are trying to understand the mechanisms underlying EGFR inhibitor resistance and discover new treatment options for patients with EGFR-driven cancers.
At the meeting, Adam Patterson, Ph.D. and Jeff Smaill, Ph.D., of the University of Auckland, New Zealand, will report that switching to low-dose tarloxotinib treatment in laboratory models of NSCLC resulted in significant regression of tumors that were progressing despite ongoing treatment with erlotinib, a first-generation EGFR TKI. These tumor models were heterozygous for EGFR whereby both wild-type (normal) and mutant (abnormal) forms of EGFR were present.
Independent research has shown that persistent wild-type EGFR signaling is associated with TKI resistance1, and patients with heterozygous EGFR-mutant NSCLC have worse outcomes following EGFR TKI therapy than those with pure mutant-EGFR disease2.
"Our research supports the hypothesis that persistent wild-type EGFR signaling within the tumor may be an important yet underappreciated mechanism of resistance to TKIs," Patterson said.
To test for the role of wild-type EGFR signaling in TKI resistance, Patterson and colleagues engineered one NSCLC model to have extra copies of the gene for wild-type EGFR. In the original parental heterozygous model, treatment with osimertinib (AZD9291), a third-generation TKI designed to "spare" wild-type EGFR, led to tumor regressions. In contrast, in the genetically engineered model with about 40% more wild-type EGFR, tumors started to regrow after initially responding to osimertinib. Tumor regrowth was brought under control upon switching to tarloxotinib treatment, which resulted in immediate and marked tumor regressions.
"Our preliminary findings suggest that tarloxotinib may be able to overcome wild-type EGFR-driven resistance to TKI therapy," Patterson said. "We believe this is related to the role of hypoxia in driving wild-type EGFR signaling within tumors coupled with the hypoxia-activation of tarloxotinib."
Using special imaging techniques, the team led by Patterson and Smaill were able to show a spatial overlap between hypoxic regions within tumors and EGFR signaling. Similarly, they were able to visualize the areas within a tumor where tarloxotinib released its TKI and found these areas to comprise the hypoxic compartment.
"Through collaboration with Dr. Angus Grey from the University of Auckland, we have for the first time demonstrated the mechanism of action of a hypoxia-activated prodrug in a human tumor model using MALDI Imaging Mass Spectrometry. This promises to be a very important technique for this field moving forward," Patterson said.
The scientists also presented data on tarloxotinib in models of SCCHN and SCCS. Across multiple cancer in vitro cell lines, tarloxotinib's TKI exhibited greater anti-proliferative activity and consistently silenced EGFR signaling to a greater extent than equimolar concentrations of cetuximab, afatinib or dacomitinib. When tested in in vivo models, tarloxotinib was more effective compared to afatinib in controlling SCCS tumor growth, and compared to cetuximab in controlling SCCHN tumor growth. A single dose of tarloxotinib significantly reduced the hypoxic compartment in a SCCHN tumor model.
"Taken all together, the data suggest that preferential activation of tarloxotinib in the hypoxic tumor microenvironment leads to reduction of the hypoxic compartment and effective silencing of EGFR signaling within the tumor," Smaill said. "Tumor-targeted activation of tarloxotinib may limit systemic side effects, and wild-type EGFR shut down may address an apparently important mechanism of TKI resistance, both potentially contributing to better outcomes for patients with EGFR-dependent cancers."
"This important translational work continues to support our ongoing proof-of-concept Phase 2 trials in patients with NSCLC and in patients with SCCHN and SCCS," said Tillman Pearce, MD, Chief Medical Officer at Threshold. "Initial PET imaging using our proprietary hypoxia imaging agent, [18F]-HX4, shows that imaging hypoxia in these tumors is possible. We hope that by combining imaging with response data we can start to determine which patients would benefit most from tarloxotinib therapy. We look forward to having preliminary results from these studies in the first half of 2016."
THLD
8k cromos en premarket y +10%
Horizon Pharma plc Announces Exceptional Third-Quarter 2015 Financial Results and Significantly Raises Full-Year 2015 Sales and Adjusted EBITDA Guidance
http://ir.horizon-pharma.com/releasedetail.cfm?ReleaseID=941224
otra farma con una forma muy ordenada de plasmar la información.
El conseso era 185,7 millones $ en revenues y han hecho 226,5 , +22%
Consenso EPS: $0.40, real $0.70 , +75% WOOOW!
HZNP
edito: premarket +15%
GALE
Galena Biopharma to Present Final GALE-401 Phase 2 Clinical Data at the 57th American Society of Hematology (ASH) Annual Meeting and Exposition
update Suntrust
https://drive.google.com/file/d/0B1gB2YESBJV7aVlROWpLbmhVLWM/view
mantienen PO 6$
AMRN
AMRN
Mucho PO pero no le sacamos ni para una caña y una tapa... Ayer se marcó un día curioso recuperando.
no termino de ver esos precios objetivos, la verdad ...
AMRN
14:30 USD Nóminas no agrícolas (Oct) 271K 180K 137K
14:30 USD Nóminas privadas no agrícolas (Oct) 268K 165K 149K
14:30 USD Tasa de desempleo (Oct) 5,0% 5,1% 5,1%
IBB... puede ser un buen día si nos arrastra el Nasdaq... veremos
