IP addresses paradoxical activation of MAPK pathway associated with RAF kinase inhibition.
Targeted cancer drug developer Ruga negotiated rights to Selexagen Therapeutics’ RAF kinase program. The firm claims the acquired technology addresses the drawbacks to BRAF inhibition as an approach to cancer therapy. Data has demonstrated that BRAF inhibition can actually induce adaptation in RAS-activated cells and promote the development of secondary skin lesions and RAS-mutated tumor growth, while triggering the paradoxical mitogen-activated protein kinase (MAPK) pathway may in addition be responsible for an escape route for drug resistance.
Ruga is exploiting a suite of in vitro and in vivo technologies to discover and develop drugs that modulate tumor-selective adaptive responses, including tumor metabolism pathways, autophagy, the endoplasmic reticulum (ER) stress response and tumor microenvironment adaptation pathways. In 2010 the firm obtained an exclusive worldwide license to a platform technology developed at Stanford University for targeting tumor-specific adaptive responses mediated through tumor metabolism and ER stress pathways.
The RAF kinase licensed in from Selexagen will complement Ruga’s existing pipeline by targeting an additional pathway used by tumor cells to proliferate, adapt, and metastatize, the firm claims. “Ruga is well positioned to meet its goal of bringing three programs into clinical development in 2013,” comments Ray Tabibiazar, M.D., president and CEO.
Selexagen is exploiting molecular modelling and structure-based drug design technologies to develop targeted cancer therapeutics.