New Research Expands Upon Prior Preclinical Studies Performed at the Hebrew University that Evaluated KAL671, an Endocannabinoid-like Molecule, in Osteoporosis
Kalytera Therapeutics, Inc., a pharmaceutical company developing a portfolio of proprietary cannabinoid and endocannabinoid-like medicines, announced at the IPWSO Conference the results of a new preclinical study that tested the skeletal effects of KAL671 in a Prader-Willi syndrome (“PWS”) animal model. The study was led by Dr. Yossi Tam, D.M.D, Ph.D., Head of the Obesity and Metabolism Laboratory at the Hebrew University of Jerusalem and a member of Kalytera’s Scientific Advisory Board.
Prader-Willi syndrome is a complex orphan genetic disorder caused by abnormalities in the 15th chromosome. Decreased bone mineral density (“BMD”) and an increased fracture risk associated with osteoporosis are common features of individuals with PWS. There are an estimated 25,000 persons living with PWS in the U.S.
KAL671 is a unique synthetic fatty acid amide and an endocannabinoid-like molecule. In a prior study also conducted at the Hebrew University, KAL671 increased bone volume density in an osteoporosis animal model. KAL671 may offer advantages over existing osteoporosis therapies, which are commonly either anti-resorptive or proformative; KAL671 is a novel treatment approach that may be both anti-resorptive and proformative.
Dr. Tam’s study compared Magel2-null mice, a mouse model that recapitulates some of the features of PWS, to wild-type control animals. Mice were administered either KAL671 (0.5 mg/kg) or a control (Vehicle) once daily for a period of six weeks. 24 hours following the last administration, researchers performed a structural analysis of the trabecular and cortical bones.
Magel2-null mice exhibited a low bone mass phenotype, resulting from reductions in trabecular number, connectivity density, and cortical thickness. Treatment with KAL671 completely prevented trabecular bone loss observed in Vehicle-treated Magel2-null mice, possibly by increasing the number of osteoblasts, the bone forming cells, and by inhibiting bone resorption and osteoclastogenesis.
“KAL671 stimulated a rise in bone volume by increasing trabecular number and thickness,” said Dr. Tam. “Importantly, the connectivity density in the trabecular bone was also significantly improved by KAL671. This study provides supports for the continued development of KAL671 as a bone anabolic and anti-resorptive agent.”
“This research contributes greatly to our understanding of osteoporosis in PWS and adds to a growing body of evidence that supports the novel antiosteoporotic properties of KAL671,” said Professor Raphael Mechoulam, Ph.D., Co-Chair of Kalytera’s Scientific Advisory Board.
Kalytera Therapeutics is developing a portfolio of non-psychoactive cannabinoid and endocannabinoid-like medicines that we believe will address large unmet market needs. Kalytera seeks to commercialize its cannabinoid therapies across a range of disease states, with an initial focus on bone health.
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