Scribe Therapeutics Reports Preclinical Data Validating its CRISPR Genome Editing and Epigenome Modifying Technologies for Addressing Cardiometabolic Disease at American Heart Association (AHA) Scientific Sessions 2024
- Scribe’s CRISPR epigenetic silencing technology, ELXR, demonstrated dramatic and sustained lowering of LDL-C by up to 67% for nearly 6 months in non-human primates – without altering DNA sequence.
- In a second program, the company’s XE gene editing technology demonstrated highly effective reduction of APOC3 and triglyceride levels by >90% in vivo.
- Additional work with XE highlighted the exceptional potency and selectivity of Scribe’s engineered CRISPR gene editing platform, demonstrating saturation of PCSK9 gene editing in the non-human primate liver with no observed off-target effects at supersaturating doses.
Excerpt from the Press Release:
ALAMEDA, Calif.–(BUSINESS WIRE)–Scribe Therapeutics Inc. (Scribe), a genetic medicines company unlocking the potential of CRISPR to transform human health, presented preclinical data on its CRISPR X-Editor (XE) and Epigenetic Long-Term X-Repressor (ELXR) technologies at the American Heart Association’s Scientific Sessions 2024.
The new data described in Scribe’s late-breaking, oral, and poster presentations showcase the highly potent, specific, and safe editing capabilities of the company’s XE and ELXR platforms. The technologies are highly engineered, programmable CRISPR-CasX nucleases with optimized activity and specificity for broad patient populations.
Notably, these data highlight Scribe’s validation of these technologies in non-human primates. This includes the durable reduction of low-density lipoprotein cholesterol (LDL-C) of up to 55% for at least a year by the XE platform and ELXR-mediated LDL-C lowering of up to 67% for nearly 6 months at therapeutically relevant doses. Additionally, the company’s XE technology demonstrates significant reduction of apolipoprotein C-III (APOC3) protein by more than 90%, triglycerides by 97%, and total cholesterol by 84% in mice.
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