NEWS.

The WHO's first global guidance on childhood obesity draws a hard line at age 10 for GLP-1 drugs, and allows them in teens only after a six-month lifestyle program fails.

Zealand Pharma's amylin analog hit its Phase 2 diabetes trial on weight, but the signal that matters is tolerability: only 1.9 percent quit for stomach side effects, versus 1.7 percent on placebo.

REDEFINE 3, the cardiovascular outcomes trial for Novo's amylin plus GLP-1 combination, is fully enrolled. Its primary objective is to prove the drug does not raise heart risk; superiority is a separate, later question. And because the comparator is placebo, not semaglutide alone, the trial cannot credit any heart benefit to the amylin half.

In mice, the queasiness that makes people quit GLP-1 drugs runs through parabrachial CGRP neurons that have nothing to do with the appetite effect. A GIP agonist or a cheap anti-emetic shut the nausea branch and left the feeding suppression intact.

A University of Pennsylvania team traced a brainstem-to-reward wire that the hormone amylin uses to suppress eating. In mice and rats, activating the laterodorsal tegmental nucleus cells that project to the ventral tegmental area was enough to cut food intake and body weight, placing part of amylin's appetite brake in the reward system rather than the classic hunger circuits.

Elamipretide (SS-31), the four-amino-acid peptide approved last year for Barth syndrome, raised litter size and rejuvenated aging eggs in mice, and pushed leftover human IVF eggs further through maturation. It worked by stabilizing mitochondria through a vitamin B6 and VEGF-A pathway.

In OUTSTAND-2, the first Phase 3 head-to-head of its kind, Hengrui's oral GLP-1 pill safiglipron matched dapagliflozin at every dose and beat it at 90 mg on blood sugar. More than three in five patients reached target, against barely one in three on the SGLT2 drug.

Reading protein fragments whole instead of chopping them first, a Cagliari team found 381 endogenous peptides in cerebrospinal fluid. One secretogranin-5 fragment dropped step by step across MS, while the mimic NMOSD showed broad peptide loss instead.

A nationwide Swedish register of 171,917 people with type 2 diabetes found GLP-1 drugs cut the common clot-type stroke by about half (HR 0.46). SGLT2 drugs showed nothing, contradicting the observational studies that credit them.

Icotrokinra, a once-daily IL-23 receptor peptide pill, held and even raised skin clearance through two years in the Phase 3 ICONIC-TOTAL study, including 89 percent complete clearance at genital sites.

Novo Nordisk built REMODEL to find out how semaglutide protects kidneys. Its three coprimary MRI endpoints came back flat, while the vascular measures and the cells lining the kidney's filtering vessels carried the signal.

A 23,938-patient database comparison finds type 2 diabetics already on a GLP-1 drug when sepsis hit died about 19 percent less often over 90 days than those on an SGLT2 inhibitor, a gap that held to a year. Most of the secondary wins fell apart once the authors corrected for testing seven outcomes at once.

A mouse study in the EMBO Journal finds that when the obese brain stops responding to leptin almost everywhere, one neuron population keeps listening, and it is defined by the receptor the entire GLP-1 weight-loss class targets. It is the cleanest anatomical hint yet for why leptin failed as a drug and GLP-1 did not.

In a 158-patient Phase 2 at EASD, the GLP-1/GIP dual ribupatide cut weight up to 20.2 percent in Chinese women with polycystic ovary syndrome and made menstrual cycles more frequent. The reproductive benefit most likely rode the weight loss rather than a direct ovarian effect, since the drug hits GLP-1 and GIP receptors, not the reproductive axis.

Boehringer and Zealand's glucagon/GLP-1 dual agonist met both goals in SYNCHRONIZE-2, but 18 percent of patients stopped for gastrointestinal side effects and the market read it as a weaker hand in a crowded field.