Lexicon Pharmaceuticals, Inc. (Nasdaq: LXRX) announced that data from the Phase 2b clinical trial of LX4211 are being presented today as a Clinical Sciences Special Report in the Emerging Therapeutics for Diabetes and Dyslipidemia section of the American Heart Association (AHA) Scientific Sessions Conference held in Los Angeles, California. The oral presentation is being delivered by Dr. Julio Rosenstock, Director of the Dallas Diabetes and Endocrine Center at Medical City, lead investigator in the recently completed study.
"The results from this trial demonstrate potential benefits of inhibiting SGLT1 in addition to the known effects of SGLT2 inhibition, not only in improving glycemic control, but also in achieving reductions in important cardiovascular risk factors such as blood pressure and body weight with an apparent favorable safety profile that will need confirmation by long-term controlled trials," said Dr. Rosenstock.
LX4211, an investigational, oral, dual inhibitor of sodium glucose co-transporters 1 and 2 (SGLT1 and SGLT2), reduces the amount of glucose that enters the bloodstream from the gastrointestinal (GI) tract by inhibiting SGLT1, the major transporter responsible for glucose absorption, and enhances glucose excretion in the urine by inhibiting SGLT2, the major transporter responsible for glucose reabsorption by the kidney. In the trial, LX4211 was tested in 299 patients with poorly controlled type 2 diabetes on metformin therapy. Patients were randomized to receive LX4211 at doses of 75 mg QD, 200 mg QD, 200 mg BID, 400 mg QD, or placebo for 12 weeks. New data presented today showed that maximal 24-hour urinary glucose excretion occurred at 200 mg QD dose, whereas maximal HbA1c reduction was obtained at the 400 mg QD dose. This suggests that dual inhibition of SGLT1 and SGLT2 offers the opportunity to achieve improved glycemic control with lower urinary glucose excretion relative to compounds that are selective for SGLT2. These findings are consistent with previous studies that indicate LX4211's inhibition of SGLT1 in the GI tract reduces post-prandial glucose levels, resulting in a lower glucose load to be filtered by the kidney.