Peptide research, regulation, discovery. Every story links to the peptide it’s about.
RSSA meta-analysis of 25 randomized trials in 8,069 people found GLP-1 drugs cut binge eating, loss of control, and emotional eating. The same drugs pushed deliberate dietary restraint up, and the authors say it is unclear whether that is healthy control or a problem.
In 500 people with type 2 diabetes, those on a GLP-1 drug had roughly a third the odds of painful neuropathy, measured with nerve conduction tests and skin biopsies, not questionnaires. The design is cross-sectional, so protection and patient selection cannot be told apart.
A study in Investigative Ophthalmology and Visual Science found that dry-eye damage drained mouse corneas of CGRP, the nerve-made peptide a whole class of migraine drugs is built to block, and that a topical CGRP eye drop resealed the ocular-surface barrier while quieting its inflammation. Blocking the same peptide was tied to lower glaucoma risk in a migraine cohort, leaving one molecule pulling two directions in the same organ.
A prospective Belgian study found children newly diagnosed with type 1 diabetes mount almost no glucagon response to dangerous lows, and the deficit deepens over 18 months.
In a TriNetX target-trial emulation of post-bariatric-surgery patients, GLP-1 starters had about two fewer kidney cancers per thousand over five years than users of four other diabetes drugs. Real, consistent, and very small.
Insulin-degrading enzyme turns out to cut GLP-1 at two sites, and a mirror-image tweak to semaglutide resisted it and lasted longer in mice, including in the central nervous system.
In Florida health records, adults who regained weight after bariatric surgery took back off about half of it on a GLP-1 drug, roughly twice the non-user figure, with no rise in side effects over a year.
A drug-target Mendelian randomization study found the GIP receptor pathway, not the GLP-1 one, lined up with the broadest slower-aging profile, and blood-sugar lowering carried more of it than weight loss.
Acute kidney injury has no drug. A small peptide copied from Klotho protected mouse kidneys through both chemotherapy and blocked-blood-flow injury by guarding one mitochondrial protein, ATAD3A, from destruction and keeping the cell-death signal contained.
Hanmi's HM17321 is an engineered urocortin-2 peptide that switches on the CRFR2 receptor instead of the incretin pathway, with a pitch of weight loss that spares muscle. Genentech bought in for up to $2.3 billion before any human efficacy data exists.
JP1, a peptide engineered to cross into the brain and home to motor neurons, eased paralysis and extended survival in SOD1 ALS mice by switching on the Nrf2 antioxidant and autophagy program. A clean knockout control pins the benefit to that one pathway, but the SOD1 mouse has a long record of wins that never reached patients.
A Japanese study found a third of GLP-1 users had inadequate bowel prep versus one in six non-users, and a 123,858-patient meta-analysis backs the direction. The weekly-versus-daily wrinkle and the right washout window are still guesswork.
MOTS-c is better known as an exercise-mimicking longevity signal. Glued into a gel and loaded with isolated mitochondria, it kept the cargo producing energy for up to 8 hours and, injected into rat hearts after a heart attack, reprogrammed macrophages and lifted pumping function from about 31 to 68 percent.
In 13,007 adults with a psychiatric diagnosis, starting semaglutide tracked with about a quarter fewer clinician-recorded cognitive signs over a year than no diabetes drug, glipizide or empagliflozin. Against sitagliptin, a pill that raises the body's own incretin hormones, the advantage vanished. Both readings of that null undercut a semaglutide-specific brain claim.
In people with atherosclerotic heart disease, helper T-cells reacted weakly to P210, a fragment of the LDL-carrying protein buried in artery plaques, and the weakness held a year later. A nanoparticle version of the peptide pulled that response back toward normal in the patients' own cells, a case for testing an atherosclerosis vaccine in people, not proof it works.