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Prime Medicine, Inc. Common Stock

Prime Medicine, Inc., a biotechnology company, engages in delivering genetic medicines to address the spectrum of diseases by deploying gene editing technology in the United States. Its lead therapeutic product candidate is PM359 for Chronic Granulomatous Disease, which is in Phase 1/2 clinical trial; PM577 for Wilson Disease, that is in preclinical studies; and PM647 to treat genetic disorder caused by mutations in the SERPINA1 gene, resulting in production of misfolded Z-AAT protein that accumulates in the liver and leads to hepatocellular injury, cirrhosis, and increased risk of hepatocellular carcinoma. The company also provides vivo programs targeting diseases of the liver, and Cystic Fibrosis programs. In addition, it offers Prime Editing technology comprising a programmable DNA binding domains, such as Cas domains, are typically modified such that they do not cause a double-stranded break in the DNA, as well as a RT domain that copies the edited DNA sequence directly into the target genomic site where the edit is made; and pegRNA which contains a search sequence, also known as a spacer, which provides a target genomic address for the Prime Editor. The company has a research collaboration and license agreement with BMS; Cystic Fibrosis Foundation; Broad Institute; and Beam. Prime Medicine, Inc. was incorporated in 2019 and is headquartered in Cambridge, Massachusetts.

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Biotech & Genomic Medicine2

Prime Medicine Wins Arbitration Ruling on PM647 Gene-Editing Drug

Prime Medicine announced a positive, binding resolution to its arbitration with Beam Therapeutics over their 2019 Collaboration and License Agreement. The Tribunal declared that PM647, the company's investigational Prime Editing drug for Alpha-1 Antitrypsin Deficiency, falls within Prime Medicine's defined field under the agreement, meaning Prime Medicine did not breach the agreement and owes no monetary damages to Beam Therapeutics. PM647 uses a universal liver lipid nanoparticle to correct the E342K mutation in the SERPINA1 gene, the most common disease-causing mutation in AATD, and has shown high editing efficiency and restored healthy-range protein levels in fully humanized mouse models at clinically relevant doses.
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Biotech & Genomic Medicine

H.C. Wainwright Upgrades Prime Medicine to Buy on Wilson’s Disease Trial Clearance

H.C. Wainwright upgraded Prime Medicine to Buy from Neutral with an $8 price target after New Zealand’s Medicines and Medical Devices Safety Authority accepted the clinical trial application for PM577a, the company’s investigational therapy for Wilson’s disease. The firm called the clearance a meaningful de-risking event, noting it marks the first clinical authorization for an in vivo prime editing therapy from Prime Medicine. The clearance, announced on June 18, 2026, enables a global Phase 1/2 study in adults and adolescents with Wilson Disease, with proof-of-concept data expected in 2027. Separately, on June 22, 2026, the FDA granted Regenerative Medicine Advanced Therapy designation to PM359, the company’s stem cell therapy for p47phox-deficient chronic granulomatous disease, based on Phase 1/2 data published in The New England Journal of Medicine.
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Biotech & Genomic Medicine

Prime Medicine Gains First Clearance for PM577a in Wilson Disease

Prime Medicine has received clearance from New Zealand's Medsafe for its Clinical Trial Application for PM577a, an investigational Prime Editing therapy targeting the H1069Q mutation in Wilson disease. This is the company's first clinical authorization for an in vivo Prime Editing therapy, allowing a global Phase 1/2 study to begin in the second half of 2026. The trial will assess safety, tolerability, and biological activity in adults and adolescents, with initial clinical data expected in 2027. PM577a is designed as a one-time therapy that corrects the genetic root cause of Wilson disease, a disorder caused by ATP7B gene mutations leading to copper buildup. Prime Medicine also noted its modular lipid nanoparticle delivery platform may enable expansion into additional mutations, including R778L, which is more common in East Asian populations.
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