Blocking a newly discovered enzyme stopped weight gain and lowered cholesterol in animal studies, opening a potential path to a three-in-one obesity drug
February 6th, 2026: Discovery gains widespread media attentionNew here? Follow stories to track developments over time. Create a free account to get updates when stories you care about change.
Scientists at University Hospitals Cleveland Medical Center and Case Western Reserve University have identified an enzyme the body needs to make fat—and when they blocked it, mice stopped gaining weight and their cholesterol dropped. The enzyme, called SCoR2, works by stripping nitric oxide from proteins that normally keep fat production in check. Remove SCoR2, and that natural brake stays engaged.
The discovery, published in <em>Science Signaling</em> in December 2025, could lead to a single drug that treats obesity, fatty liver disease, and cardiovascular disease simultaneously. Over 1 billion people are classified as obese globally, and the economic toll is projected to hit $4 trillion annually by 2035. A new mechanism for blocking fat production would expand therapeutic options beyond appetite-suppressing GLP-1 drugs.
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Fictional AI pastiche — not real quote.
"A fine discovery, this enzyme switch! Though I observe that Nature gives us hunger to make us work, and now Science offers to make us thin whilst we sit idle. I suspect the greatest benefit will be to those who can afford both the feast *and* the cure—a modern alchemy that turns gold into slenderness."
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A nonprofit institute that accelerates academic discoveries through the high-risk stages of drug development by providing funding, pharmaceutical expertise, and business development support.
A private research university in Cleveland with strong programs in medicine and biomedical engineering, frequently collaborating with University Hospitals on translational research.
October 1998 February 2026
Science Daily and other outlets reported on the SCoR2 findings, highlighting the potential for a new class of obesity drugs targeting fat production rather than appetite.
Stamler's team published findings in <em>Science Signaling</em> identifying SCoR2 as an enzyme required for fat production, showing that blocking it prevented weight gain and lowered cholesterol in mice.
The FDA approved semaglutide as the first GLP-1 therapy indicated for MASH, expanding the proven applications of obesity drugs to liver disease.
The FDA approved resmetirom (Rezdiffra) as the first drug specifically indicated for metabolic dysfunction-associated steatohepatitis, demonstrating demand for liver-targeted obesity treatments.
The FDA approved Wegovy (semaglutide 2.4mg) for chronic weight management, marking a turning point in obesity pharmacotherapy with a GLP-1 receptor agonist achieving significant weight loss.
Jonathan Stamler established the Harrington Discovery Institute at University Hospitals Cleveland Medical Center to accelerate translation of academic discoveries into drugs.
Robert Furchgott, Louis Ignarro, and Ferid Murad won the Nobel Prize in Physiology or Medicine for discovering nitric oxide as a cardiovascular signaling molecule, establishing the scientific foundation for understanding NO's role in metabolism.
3 moments from history that rhyme with this story — and how they unfolded.
The FDA requested withdrawal of fenfluramine and dexfenfluramine from the market after reports linked the combination to heart valve damage. At its peak, over 18 million prescriptions were written annually. About 30% of users showed abnormal echocardiograms even without symptoms.
Manufacturer American Home Products (later Wyeth) eventually paid over $13 billion in legal damages to affected patients.
The FDA significantly tightened cardiovascular safety requirements for obesity drugs, requiring long-term outcome studies before approval and creating lasting skepticism about weight-loss medications.
Any new obesity drug mechanism faces heightened scrutiny for cardiovascular effects. The SCoR2 inhibitor's cholesterol-lowering action will need extensive cardiac safety data given this history.
Robert Furchgott, Louis Ignarro, and Ferid Murad shared the Nobel Prize in Physiology or Medicine for discovering that nitric oxide—a gas and free radical—functions as a critical signaling molecule in the cardiovascular system, controlling blood vessel dilation.
The prize validated decades of research and accelerated pharmaceutical interest in nitric oxide pathways, contributing to drugs like sildenafil (Viagra).
Stamler's subsequent work on S-nitrosylation—how NO attaches to proteins—built directly on this foundation, eventually leading to the SCoR2 discovery 27 years later.
The SCoR2 finding represents a new chapter in nitric oxide research, showing the molecule's role extends beyond blood vessels to fat metabolism.
The FDA approved semaglutide 2.4mg (Wegovy) for chronic weight management in adults, marking the first new obesity drug in seven years. Trial participants lost an average of 15% of body weight, far exceeding previous medications.
Demand vastly outstripped supply, creating shortages that persisted for years. Novo Nordisk's market capitalization surged past $400 billion.
GLP-1 agonists transformed obesity from a condition with limited pharmaceutical options to one with multiple effective treatments. By 2025, the class generated over $39 billion in annual revenue.
The SCoR2 inhibitor would enter a market transformed by GLP-1 success. It offers a different mechanism—blocking fat production rather than suppressing appetite—which could serve patients who don't respond to or can't tolerate GLP-1 drugs.