Peptide research, regulation, discovery. Every story links to the peptide it’s about.
RSSA meta-analysis of 20 studies and 546,668 patients found no rise in eight surgical complications for GLP-1 drug users after spine surgery, and about 50 percent higher odds of a successful bone fusion.
A pooled analysis of five studies and 1,186 people with metastatic neuroendocrine cancer found that removing the primary tumor before peptide receptor radionuclide therapy tracked with 38 percent lower progression risk (HR 0.62) and 54 percent lower death risk (HR 0.46). The authors call it an association, not proof, and name the two biases that could explain it.
Kids carrying one version of the GLP1R gene, the target Ozempic hits, were more insulin-sensitive and made less GLP-1, before any drug. An association, not a prescription.
COURAGE-2, a Phase 3 trial published July 16 in the Journal of Clinical Neuroscience, gave 188 acute ischemic stroke patients standard care or standard care plus intravenous EGF and GHRP-6, a growth-hormone-releasing peptide. In the full population it missed its primary endpoint: no difference in disability, function, or survival. Among the 27 most severe strokes (NIHSS 15 and up) the treated patients were less disabled at six months (Rankin 2.6 vs 4.7) and far less likely to die (HR 0.18). A subgroup that small, carved out after a flat main result, is a lead for a future trial, not a verdict.
A glucagon-receptor antibody raised sperm counts and motility in diabetic, aged, and healthy mice by restoring a lactate fuel line that glucagon had been throttling inside the testis.
Inspired by spider silk, a self-assembling peptide folded into nanofibers around glioma mitochondria and, under ultrasound, produced 3.7 times more of a cell-killing molecule than the loose peptide.
SS-31, a mitochondrial peptide already cleared for a rare heart disease, cut the share of irradiated heart-muscle cells showing an aging marker from 67 percent to 38 percent.
Most STING research tries to switch the innate-immune alarm on to fight cancer. A docking screen of 59,319 peptides went the other way and found one, Peptide-1, that binds STING at 0.15 micromolar and quiets cGAMP-driven inflammation in mouse macrophages. It is the mirror image of a peptide we covered last month.
MAX-7 degrades the cancer master-switch MYC through chaperone-mediated autophagy, bypassing the proteasome that most targeted degraders use, and shrank triple-negative breast tumors in mice.
In colorectal cancer cells and mice, the stapled peptide i7-01s-20 reactivated Beclin1 and degraded both EGFR and beta-catenin at once, and the effect vanished when Beclin1 was silenced.
Mephedrone built a place preference in rats only when dosed socially, not alone. Blocking that reward took opposite moves on two peptide receptors: turning the oxytocin receptor up (carbetocin) or the vasopressin V1A receptor down (SR49059). Peripheral vasopressin did nothing, so the switch is central.
Integrins share the same RGD binding address, so PET probes built on it cannot tell the subtypes apart. A Journal of Medicinal Chemistry study tuned the shape of cyclic RGD peptides instead of their sequence, building a 25-member ring library. Two of three lead probes imaged their target integrin in tumor-bearing mice; the third stayed selective in cells but failed in the animal.
GLP-1 drugs slow the stomach, and food left behind before an upper endoscopy can be inhaled under sedation. A retrospective study of 16,067 scopes found that keeping the drug on board raised the odds of retained stomach contents about tenfold, while a two-week hold brought them back near normal. Obese patients stayed high-risk even after holding.
A TriNetX records study published July 7 in the American Journal of Physical Medicine and Rehabilitation found that spinal cord injury patients started on a CGRP inhibitor were less likely to need a gabapentinoid within a month than those started on topiramate (odds ratio 0.62) or propranolol (0.75). CGRP is the pain-signaling peptide these migraine antibodies block, and it sprouts abnormally in the injured spinal cord, giving the repurposing idea a mechanism. It is an association, not a trial.
The full phase 3 TRANSCEND data published July 9 in the New England Journal of Medicine: setmelanotide dropped body-mass index 16.5 percent over a year in acquired hypothalamic obesity while placebo gained 3.3 percent. Read against Rhythm's EMANATE failure in partial-loss obesity two months ago, it draws a clean line: the MC4R agonist works only where the melanocortin satiety circuit is fully broken, whether a mutation silenced it or a tumor destroyed the tissue around it.