Enable Medicine Announces Publication in Science Immunology Showing Spatial Transcriptomics Reveal Distinct Mechanisms of Response to Psoriasis Therapy
29 Jan 2024
- High-resolution molecular portraits of IL-23 blockade in cutaneous psoriasis using Enable’s multimodal atlas of human disease can guide better treatment decisions.
- Enable partnered with academic institutions to identify the molecular drivers of IL-23 blockade therapy in psoriasis.
MENLO PARK, Calif.--(BUSINESS WIRE)-- Enable Medicine, a leader in AI for biological research and drug discovery, announced today a research publication in Science Immunology that details a high-resolution spatial and transcriptomic atlas of IL-23 blockade in skin which provides insight on how different drug classes reprogram pathologic inflammation.
The study led by Enable Medicine in collaboration with academic partners at UCSF, utilized Enable’s single-cell transcriptomic analysis and spatial transcriptomics platform to unravel the complex molecular landscape of psoriatic lesions before and during treatment with the anti-IL-23 biologic tildrakizumab.
The paper titled: "A single-cell atlas of IL-23 inhibition in cutaneous psoriasis distinguishes clinical response," details crucial insights into the mechanisms underlying treatment response and resistance in psoriasis patients receiving IL-23 blockade. Psoriasis vulgaris and other chronic inflammatory diseases improve markedly with therapeutic blockade of IL-23 signaling, but the genetic mechanisms underlying clinical responses remain poorly understood. Using single cell transcriptomics, researchers profiled immune cells isolated from lesional psoriatic skin before and during IL-23 blockade.
Enable Medicine’s multimodal atlas of human disease was able to perform the indexing, annotation, and analysis of biological data points at scale, utilizing proprietary generative AI models alongside state-of-the-art algorithms.
“This high-resolution spatial and transcriptomic atlas of IL-23 blockade in skin provides a fundamental step forward in understanding how a predominant drug class reprograms pathologic inflammation. The resulting data has implications for more precisely targeting therapies in chronic diseases of the skin, joint, and gut,” said Raymond Cho, MD, PhD, a co-author of the paper and Associate Professor of Dermatology, UCSF. “By uncovering the complex interplay between immune cells, cytokines, and keratinocytes in psoriatic lesions, we can develop better personalized treatments that address the heterogeneous nature of the disease and improve patient outcomes."
“This study offers unprecedented insights into the molecular mechanisms underlying treatment response and resistance in psoriasis. By elucidating the cellular and transcriptional dynamics of psoriatic lesions during IL-23 blockade therapy, this research paves the way for the development of more targeted and effective therapeutic strategies for patients with psoriasis,” said Aaron Mayer, Co-Founder and Chief Scientific Officer, Enable Medicine, and co-author on the paper.
Psoriasis vulgaris (PV) affects over 100 million individuals globally, imposing a significant burden on patients' lives. Among the novel therapeutic strategies developed for psoriasis management, anti-IL-23 medications have emerged as the current standard of care. However, despite their efficacy, a substantial portion of patients—10-20%—do not respond adequately to these treatments. A better understanding of the mechanisms of actions behind certain therapies and the fundamental drivers of disease affecting drug resistance and treatment response are needed.
About Enable Medicine
Enable Medicine harnesses the revolutionary capabilities of AI to provide cutting-edge insights into biology and medicine. Our platform finds biological signatures relevant to the asset or indication. Our global network of partners leverage the platform to guide target discovery, identify new biomarkers, and develop optimal treatment strategies. Enable Medicine is headquartered in Menlo Park, CA. Learn more at: . Follow us @EnableMedicine.
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