ARIAD ist wieder in the Game (was hier aber die meisten eh schon geahnt haben - spätestens seit dem 8.11.)...
Es würde nun auch wieder Zeit werden, die nächsten Schritte von ARIAD abzuschätzen.
Da Iclusig aller Wahrscheinlichkeit nach auch Fond der FDA ein positives Votum erhalten wird (keine Alternative - benefits outweigh risks), könnte nun auch die restliche Pipeline ins Blickfeld geraten und für Kurssprünge sorgen --> denn das Geld für die hauseigene Forschung ist gesichert!
M.E. wird das hier für grosse Wellen sorgen:
ARIAD scientists identified multiple compounds that potently inhibit ALK both in vitro and in vivo while maintaining significant selectivity over the highly homologous insulin-like growth factor-1 receptor and insulin receptor tyrosine kinases. Based on proprietary ARIAD chemistry, AP26113 was identified as the lead compound—in in-vitro studies it potently inhibited ALK-expressing tumor cells while having no effect on ALK-negative cells. In addition, this compound was active when administered orally in multiple mouse models of lymphoma and lung cancer with minimal effects on insulin or glucose levels.
In 2010, ARIAD announced results of preclinical studies on AP26113 showing potent inhibition of the target protein, including mutant forms that are resistant to the first-generation ALK inhibitor, crizotinib. ARIAD scientists presented these data at the annual meeting of the American Association for Cancer Research (AACR) in Washington, D.C. Read the Press Release.
ARIAD scientists used an in vitro assay to identify mutations in ALK that confer resistance to the dual Met/ALK inhibitor developed by Pfizer, Inc., crizotinib, or to AP26113. This resistance-profiling method has successfully predicted the specific mutations that confer clinical resistance to other tyrosine kinase inhibitors, such as the BCR-ABL inhibitors used in chronic myeloid leukemia (CML). Multiple mutations in ALK were identified that conferred resistance to crizotinib, but not to AP26113. Three of these ALK mutants were also tested in mouse tumor models, and in each case, AP26113 potently blocked tumor growth while crizotinib was ineffective.
In a second study, ARIAD performed direct comparative studies on AP26113 and crizotinib in a series of ALK-dependent cell culture and in vivo models. In all models, AP26113 was at least ten-fold more potent than crizotinib. In addition, AP26113 exhibited approximately 100-fold selectivity for ALK-positive cell lines compared with an approximate 10-fold selectivity for crizotinib, and demonstrated encouraging pharmacologic properties, including the potential for once-daily oral dosing.
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Alleine der letzte Absatz lässt jeden Investor obgleich des Potentials in 3D träumen... Kurse von $20 und darunter erschienen dann nicht nur untertrieben, sondern schon fast lachhaft.
GLTA
GLTA |
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