Azome Therapeutics Presents at 7th Annual Inflammasome Therapeutics Summit
- N-Vision Accounts
- Nov 7
- 1 min read
November 6, 2025
Azome Therapeutics CEO Elliott Gruskin and the Head of the company’s Scientific Advisory Board Rashmin Savani were among the expert speakers at the 7th Annual Inflammasome Therapeutics Summit – the leading industry forum dedicated exclusively to inflammasome-targeted drug development – held November 4-6 in Boston, MA
As one of the summit’s keynote speakers, Dr. Savani discussed the development of the company’s novel RHAMM-targeted antagonist technology. His presentation demonstrated how the company’s peptides and small molecule inhibitors effectively block RHAMM-target interactions required for activation of the NLRP3 inflammasome to support precise immune modulation.
This year’s summit also featured Azome’s Gruskin in a fireside chat with CEOs on addressing stakeholder needs and positioning inflammasome therapies for clinical, commercial and capital success.
Azome’s novel RHAMM (Receptor for Hyaluronan-Mediated Motility) antagonist technology platform and its lead drug candidate, AZM-152, which blocks inflammasome activation, has demonstrated excellent potential for advancing the treatment of severe inflammatory diseases, including several with significant unmet needs. Last November, the company announced that it had entered into a Cooperative Research and Development Agreement (CRADA) with the National Center for Advancing Translational Sciences (NCATS) to investigate AZM-152 in bronchopulmonary dysplasia (BPD).
About Azome Therapeutics
Azome Therapeutics is focused on developing selective RHAMM antagonists of the NLRP3 inflammasome, an inflammatory pathway critical to the development of a wide variety of diseases, including acute lung injury, acute respiratory distress syndrome, bronchopulmonary dysplasia, systemic sepsis, acute liver and kidney injury, and pneumonia. The company’s lead candidate, AZM-152, is a RHAMM-derived antagonist that blocks key priming and activation signals involved in the aberrant activation of the NLRP3 inflammatory cascade.