Data supports continued development of XOMA 129 as a novel targeted therapy for the treatment of hypoglycemic conditions

BERKELEY, CA, USA I April 04, 2016 I XOMA Corporation (Nasdaq:XOMA), a leader in the discovery and development of therapeutic antibodies, announced the presentation of data from XOMA 129, the lead compound in the Company’s XMetD antibody fragment (Fab) program, at the Endocrine Society’s Annual Meeting — ENDO 2016. A senior scientist at XOMA presented the Company’s poster titled “XOMA 129, a Novel Insulin Receptor Negative Modulator, is Efficacious in Treating Insulin- and Glibenclamide-induced Hypoglycemia in Animals.”

“Severe acute hypoglycemia is a common complication with diabetes therapies that requires prompt recognition and treatment to prevent severe toxicity and potentially mortality. XOMA 129, our novel Fab that binds to an allosteric site on the insulin receptor, was designed to have a rapid onset and limited duration of action, two important clinical requirements in reversing an acute hypoglycemic event,” stated Paul Rubin, M.D., Senior Vice President, Research and Development, and Chief Medical Officer at XOMA. “The data presented at ENDO 2016 demonstrate our Fab exhibits the rapidity of effect and clearance traits required, thereby leading us to believe XOMA 129 represents a novel potential treatment approach for these severe hypoglycemic episodes.”

The poster outlines XOMA 129’s performance in separate pre-clinical models: cell culture and animal pharmacology studies. In vitro assays showed XOMA 129 decreases the activity of insulin on mammalian cells over-expressing human, rat and minipig insulin receptor (INSR) in a dose-dependent manner. Further studies confirmed XOMA 129 binds to the INSR and acts as a negative allosteric modulator. In animal studies, potential rescue of insulin or sulphonylurea-induced hypoglycemia was modeled in normal rats. Administration of insulin or glibenclamide (a sulfonylurea) produced abnormally low glucose levels. Intravenous administration of XOMA 129 at time points wherein the drug-induced glucose levels were falling below normal levels rapidly stabilized blood glucose levels thereby preventing hypoglycemia. In normal minipigs, intramuscular administration yielded significant elevation of blood glucose lasting for several hours thereby confirming the activity in mammals.

About XOMA 129

XOMA 129 is a fully human, high affinity monoclonal antibody fragment that specifically targets the human insulin receptor (INSR). Insulin is the major hormone for lowering blood glucose levels. Profound hypoglycemia (low blood sugar) can result in significant morbidities, including organ damage and potentially death. There are acute and more persistent hypoglycemia conditions associated with abnormally high insulin levels, which represent unmet medical needs. As a negative allosteric modulator, XOMA 129 binds with high affinity to a site distinct from insulin binding and dampens insulin signaling. This drug candidate has been designed to provide a rapid onset of action and a duration of action tailored to meet the pharmacotherapy needs in certain conditions. The Company intends to pursue an Investigational New Drug (IND) application in the US for XOMA 129 upon completion of its IND-enabling nonclinical development activities.

About XOMA Corporation

XOMA Corporation is a leader in the discovery and development of therapeutic antibodies. The Company’s innovative product candidates result from its expertise in developing ground-breaking monoclonal antibodies, including allosteric antibodies, which have created new opportunities to potentially treat a wide range of human diseases. XOMA’s scientific research has produced a portfolio of five endocrine assets, each of which has the opportunity to address multiple indications. The Company’s lead product candidate, XOMA 358, is an allosteric monoclonal antibody that reduces insulin receptor activity, which could have a major impact on the treatment of hyperinsulinism. The Company recently initiated Phase 2 development activities for XOMA 358 in patients with congenital hyperinsulinism. For more information, visit www.xoma.com.

SOURCE: XOMA