ZyVersa Therapeutics Presents Groundbreaking Research Supporting Potential of Inflammasome ASC Inhibitor IC 100 in Treating Parkinson's Disease
PorAinvest
martes, 29 de abril de 2025, 1:06 pm ET1 min de lectura
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The study was conducted by researchers at the University of Miami Miller School of Medicine, supported by a grant from the Michael J. Fox Foundation. The findings suggest that IC 100, a novel humanized IgG4 monoclonal antibody, could be a promising disease-modifying therapy for PD. The study highlights that IC 100 uniquely targets the inflammasome adaptor protein ASC and multiple types of inflammasomes, including NLRP1, NLRP2, NLRP3, NLRC4, AIM2, and Pyrin.
The study's lead author, Dr. Robert W. Keane, Professor of Physiology and Biophysics at the University of Miami, noted that the findings demonstrate the potential of targeting inflammasomes and ASC specks not only for PD but also for Lewy body dementia (LBD) and Alzheimer’s Disease. IC 100’s mechanism, which inhibits both ASC speck activity and misfolded protein aggregates, makes it a strong candidate for treating neurodegenerative diseases.
ZyVersa Therapeutics plans to initiate proof-of-concept studies in animal models later this year, building on the promising preclinical data. The company is well-positioned in the rapidly emerging inflammasome space with IC 100 and in kidney disease with phase 2 Cholesterol Efflux Mediator™ VAR 200. The total accessible market for these indications is over $100 billion.
References:
[1] https://www.globenewswire.com/news-release/2025/04/29/3070085/0/en/ZyVersa-Therapeutics-Announces-Published-Data-Showing-Inflammasome-ASC-Inhibitor-IC-100-Decreases-Microglial-Inflammasome-Activation-and-Alpha-Synuclein-That-Contribute-to-Neurodeg.html
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ZyVersa Therapeutics has published data supporting the potential of its Inflammasome ASC Inhibitor IC 100 to slow Parkinson's disease progression. The study, published in npj Parkinson's Disease, shows that IC 100 blocks microglial inflammasome activation and reduces neurotoxic alpha-synuclein accumulation, key contributors to PD progression. The company plans to initiate proof-of-concept studies in animal models later this year.
ZyVersa Therapeutics, Inc. (Nasdaq: ZVSA) has published significant data supporting the potential of its Inflammasome ASC Inhibitor IC 100 to slow the progression of Parkinson’s disease (PD). The study, published in npj Parkinson's Disease, a peer-reviewed journal from Nature, demonstrates that IC 100 blocks microglial inflammasome activation and reduces neurotoxic alpha-synuclein accumulation, both key contributors to PD progression.The study was conducted by researchers at the University of Miami Miller School of Medicine, supported by a grant from the Michael J. Fox Foundation. The findings suggest that IC 100, a novel humanized IgG4 monoclonal antibody, could be a promising disease-modifying therapy for PD. The study highlights that IC 100 uniquely targets the inflammasome adaptor protein ASC and multiple types of inflammasomes, including NLRP1, NLRP2, NLRP3, NLRC4, AIM2, and Pyrin.
The study's lead author, Dr. Robert W. Keane, Professor of Physiology and Biophysics at the University of Miami, noted that the findings demonstrate the potential of targeting inflammasomes and ASC specks not only for PD but also for Lewy body dementia (LBD) and Alzheimer’s Disease. IC 100’s mechanism, which inhibits both ASC speck activity and misfolded protein aggregates, makes it a strong candidate for treating neurodegenerative diseases.
ZyVersa Therapeutics plans to initiate proof-of-concept studies in animal models later this year, building on the promising preclinical data. The company is well-positioned in the rapidly emerging inflammasome space with IC 100 and in kidney disease with phase 2 Cholesterol Efflux Mediator™ VAR 200. The total accessible market for these indications is over $100 billion.
References:
[1] https://www.globenewswire.com/news-release/2025/04/29/3070085/0/en/ZyVersa-Therapeutics-Announces-Published-Data-Showing-Inflammasome-ASC-Inhibitor-IC-100-Decreases-Microglial-Inflammasome-Activation-and-Alpha-Synuclein-That-Contribute-to-Neurodeg.html

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