SGX Initiates Phase I Trials For SGX523
SGX Pharmaceuticalst has opened enrollment in two Phase I studies. The Phase I studies are designed to evaluate the safety, tolerability and pharmacokinetic profile of SGX523, an internally developed, orally-bioavailable, small molecule inhibitor of the cMET receptor tyrosine kinase.
The Phase I clinical trials are open-label, dose escalation studies of SGX523 administered orally to patients with advanced cancer who have either failed standard therapy or for whom no standard therapy exists. The studies are designed to explore two dosing regimens in parallel. The continuous dosing trial will have continuous uninterrupted twice daily dosing with patients being evaluated every 28 days for continuation of treatment. The intermittent dosing schedule will implement twice daily dosing on a 14 days on/7 days off therapy schedule, cycling every 21 days. In both protocols, patients may continue on therapy for up to 12 months as determined by the patient's response and tolerance to SGX523.
"SGX523 is our first internally discovered clinical candidate. We are excited to begin studying SGX523 in humans and to achieve the first of our 2008 clinical development goals," said Mike Grey, President and Chief Executive Officer of SGX Pharmaceuticals. "With two separate dosing schedules, we believe that we will be able to collect important data that could serve as a basis for future clinical development activities and position us to capitalize on the evolving cMET opportunity."
About SGX523 and cMET
SGX523 has shown exceptional selectivity for the cMET receptor tyrosine kinase over more than 200 protein kinases and has demonstrated both potent in vitro blockage of the activity of this cancer target and in vivo activity against various types of human cancer cells that depend on cMET for their uncontrolled growth and proliferation. The cMET receptor tyrosine kinase has been implicated in a wide range of cancers, including both solid and blood tumors. cMET has been extensively studied in the laboratory environment and, to a lesser extent, in the clinic, with increasing data suggesting that uncontrolled stimulation of cMET plays a key role in a variety of effects associated with cancer, including cellular growth, increased cell movement and invasion, and an increased ability of cancer cells to metastasize. Other observations have implicated cMET in increased angiogenesis. cMET activation has been observed in a wide range of other cancer types including breast, colon, prostate, pancreatic and gastric cancers.