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Daily Briefing · September 28, 2026

Today's Peptide News — September 28, 2026

Viking's VK2735 holds up to 97% of weight loss on less frequent dosing, Novo plans a tenfold oral Wegovy scale-up, and a single-dose CRISPR therapy halves LDL cholesterol.

Tirzepatide Batokine Release: Brown Fat Activation Beyond Reduced Eating in Obese Mice

A University of Barcelona team reports in Biomedicine & Pharmacotherapy that tirzepatide, the dual GIP/GLP-1 receptor agonist, activates brown adipose tissue in obese mice beyond what eating less explains. The study used pair-fed controls, so differences between groups reflect the drug rather than reduced intake. This is the same paper covered in yesterday's digest and remains the most recent peptide-specific primary study surfaced in the past few days.

Why it matters: it suggests incretin-based peptides may influence energy expenditure and brown-fat signaling molecules called batokines, not only appetite. The evidence is from mice, and human brown fat biology differs, so this is hypothesis-generating.

Suggested PeptideWiki angle: a short explainer on batokines and what pair-feeding controls can and cannot tell us, framed as a follow-up to any tirzepatide post. If you already published on this paper, treat this as optional.

Viking Therapeutics VK2735 Keeps Up to 97 Percent of Weight Loss With Less Frequent Dosing

Viking Therapeutics reported maintenance-study data for VK2735, an injectable GLP-1/GIP dual agonist. Participants on 17.5 mg weekly lost an average of 17.7 percent of body weight over 21 weeks, and weight loss continued through week 33 without a plateau. After switching to less frequent dosing, up to 97 percent of the loss was retained with every-other-week injections and about 90 percent with monthly dosing.

Gastrointestinal adverse events during maintenance were comparable to placebo. Analysts called the readout a best-case scenario following a disappointing oral formulation trial in 2025, and Viking shares rose more than 30 percent.

Novo Nordisk Plans Tenfold Expansion of Oral Wegovy Manufacturing by 2030

Novo Nordisk said it will scale oral Wegovy manufacturing to ten times the number of patients it serves today, currently about 1.5 million. The company plans to grow its total patient base from 46.5 million to more than 60 million by the end of the decade.

Capacity will come from existing domestic sites, including a repurposed plant in Ireland and expanded operations in Durham, North Carolina, with third-party manufacturing under consideration. Novo also plans launches in more than 20 markets by 2027.

Novo Nordisk to Present Wegovy Pill and Next-Generation Amylin Data at EASD 2026

Novo Nordisk announced it will share real-world and clinical data on the Wegovy pill, along with progress on its next-generation amylin treatments, at the EASD 2026 meeting. Only the announcement headline was reviewed for this digest, so specific results should be checked once presented.

Amylin analogues are an increasingly watched peptide class as a partner to GLP-1 therapy, which makes the EASD readouts worth monitoring for PeptideWiki content.

CRISPR Therapy CTX310 Cuts LDL Cholesterol by About Half in a Single Dose

A single infusion of the experimental CRISPR-Cas9 therapy CTX310, which disables the ANGPTL3 gene in the liver, reduced LDL cholesterol by 52.5 percent and triglycerides by 47.8 percent at the highest dose after one year in 15 patients with treatment-resistant lipid disorders. No serious adverse events were reported.

The study was published in the New England Journal of Medicine, led by Cleveland Clinic, and funded by CRISPR Therapeutics. It is a small early-stage trial.

Glucosamine Use Linked to Faster Progression From Mild Cognitive Impairment to Dementia

Researchers at the University of Florida, publishing in Nature Metabolism, found that glucosamine users with mild cognitive impairment had a 25 percent higher likelihood of progressing to dementia, based on health records from 2012 to 2024 plus lab work in human brain tissue and mouse models.

The authors stress the finding is an association, not proof of causation, and that human trials are needed before anyone changes supplement use. The proposed mechanism involves excessive sugar-tagging of proteins in Alzheimer's brains.