Azome Therapeutics Presents at 7th Annual Inflammasome Therapeutics Summit

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 7^th 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.

Azome Therapeutics Featured at Hyaluronan 2025

October 9, 2025

Dr. Rashmin Savani, the Head of Azome Therapeutic’s Scientific Advisory Board, was a featured speaker at this summer’s 15th conference of the International Society for Hyaluronan Science (Hyaluronan 2025) held June 8-12 in St. Charles, IL.

Dr. Savani, a leading expert in the biology of preterm lung development, injury and repair, was invited to present on the latest scientific insights into the role of NLRP3 inflammasome activation and the development of bronchopulmonary dysplasia.  BPD, a chronic lung disease, is common among preterm infants where respiratory failure is treated with ventilator and oxygen therapy. 

During the conference, Azome Therapeutics also presented three scientific posters including one on hyaluronan as a predictive biomarker of death and BPD in preterm infants with respiratory failure.  Additional poster presentations focused on NLRP3 inflammasome activation in an animal model of sepsis and the integral role of RHAMM ((Receptor for Hyaluronan-Mediated Motility) in the activation of the NLRP3 inflammasome.

The company’s novel RHAMM 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, Azome 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, the company’s novel inflammasome antagonist, in BPD.

“It was an honor to be invited to speak at Hyaluronan 2025 and have this prestigious opportunity to share the findings from our research with other society members,” said Dr. Savani. “Based on our early data, we are very hopeful that our novel, first-in-class therapy will one day help the thousands of families affected by BPD, one of the most common chronic lung diseases of childhood for which there are no current therapeutic options and no effective means of prevention.”

About Azome Therapeutics

Azome Therapeutics is focused on developing selective 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 upstream priming and activation signals involved in the aberrant activation of the NLRP3 inflammatory cascade.

Azome Therapeutics Enters into CRADA with National Center for Advancing Translational Sciences to investigate novel inflammasome antagonist to prevent Bronchopulmonary Dysplasia

Collaboration focuses on studies of AZM-152 to enable submission of an Investigational New Drug (IND) application for the prevention of BPD in preterm infants

November 13, 2024 via PR Newswire

MALVERN, PA (11/13/24) - Azome Therapeutics, an early-stage drug development company, today announced that it has entered into a Cooperative Research and Development Agreement (CRADA) with the National Center for Advancing Translational Sciences (NCATS) to investigate AZM-152, the company’s novel inflammasome antagonist, in bronchopulmonary dysplasia (BPD).

Under the terms of the agreement, NCATS, part of the National Institutes of Health, will collaborate with Azome Therapeutics to perform preclinical development studies of AZM-152 to enable the submission of an Investigational New Drug (IND) application for the prevention of BPD in preterm infants.

“We are honored to have been selected by NCATS for this important research collaboration, and excited that they share our vision for AZM-152 as a potential preventative therapeutic for BPD,” said Rashmin Savani, MBChB, Chairman of Azome’s Scientific Advisory Board.

Bronchopulmonary Dysplasia (BPD) is a severe lung condition that affects 30-50% of preterm infants weighing less than 1000 grams. It develops due to ventilator and oxygen-induced damage to immature lungs, leading to an inflammatory response that results in abnormal lung development with decreased alveolarization. Approximately 15,000 infants develop BPD each year in the United States, and 10-15% of them die in the first year of life. In addition to the direct impacts on the infant and the toll this disease takes on families, healthcare expenditure has been estimated at $5B per year.

AZM-152 is a potent and specific antagonist that blocks activation of the inflammatory process that causes BPD. This inflammatory pathway, the NLRP3 inflammasome, is critical to the development of a wide variety of other diseases in addition to BPD. AZM-152 selectively blocks an essential component of the signaling pathway (the receptor for hyaluronan-mediated motility, or RHAMM) that results in aberrant NLRP3 inflammasome activation.

Previous preclinical studies in BPD have demonstrated that when AZM-152 is given as a single dose to neonatal mice exposed to hyperoxia, no inflammatory response is observed, and lung alveolarization is preserved. This preclinical finding has raised the possibility of the prevention of BPD.

“It is our hope that this novel, first-in-class therapy will one day help the thousands of families affected by this most common chronic lung disease of childhood, for which there are no current therapeutic options and no effective means of prevention,” added Azome Therapeutics CEO Elliott Gruskin, PhD.

About Azome Therapeutics

Azome Therapeutics is an early-stage drug development company focused on developing selective antagonists of the NLRP3 inflammasome, an inflammatory pathway critical to the development of a wide variety of diseases, including BPD, acute lung injury, acute respiratory distress syndrome, systemic sepsis, acute liver and kidney injury, and pneumonia. The company’s lead candidate, AZM-152, is a RHAMM-derived antagonist that blocks key upstream priming and activation signals involved in the aberrant activation of the NLRP3 inflammatory cascade.