Peptide research, regulation, discovery. Every story links to the peptide it’s about.
RSSTirzepatide activates the GIP receptor. MariTide blocks it. Both cause weight loss, and the field cannot say which is right. A new mouse study built a single peptide that does both in sequence, and the on-then-off design dropped body weight 21.6 percent, against 14.5 percent for a pure blocker.
A protein called CAP builds up in the gut of children with Hirschsprung disease and stalls the nerve cells that should colonize the colon. A fragment of that same protein, PDCAP, competes it off, and in two mouse models it let the missing nerves form.
Six phase 1 studies mapped orforglipron's drug interactions. A CYP3A4-blocking antibiotic raised the oral GLP-1 drug's levels, an epilepsy drug lowered them, and orforglipron barely touched other drugs. The injectable peptides carry no such map.
A two-photon imaging study in mouse cortex found that a small set of neurons carrying the substance P receptor drive local blood flow by releasing nitric oxide. Astrocyte calcium surges, long suspected as a cause, arrived after the vessels had already widened.
In ten adults with type 2 diabetes, a glucose drink raised blood flow through the main intestinal artery by 57 percent. Infusing a GIP-receptor blocker cut that surge about 15 percent (p=0.012), pinning a vascular job on the gut hormone tirzepatide is built around.
A real-world study in the NIH All of Us database compared the two most common migraine preventives and found the newer CGRP antibodies were non-inferior to Botox for stroke risk, though the event count was small.
Chemists built a six-amino-acid peptide called RKLAHE around a manganese ion, then used the particle to force cancer cells to leak their own mitochondrial DNA. The leak switches on the cGAS-STING pathway, the cell's alarm for misplaced DNA, and in mice with breast cancer the particle made an anti-PD-L1 immunotherapy work better. It is a mouse-stage result, but the design logic is the point.
Neurotensin, known as a brain-and-gut peptide, turned out to be produced by the heart's own lymphatic vessels after injury, where it braked muscle thickening and scarring through the NTSR2 receptor. A selective agonist reproduced the effect in mice and in human heart-failure tissue.
A four-amino-acid peptide called CAQK, given by IV, concentrated at the lesion and left treated rats using the injured forelimb close to normal (median 7 of 9 versus 3) while cutting glial scarring. Small and preclinical, and a test of delivery-first peptide design.
FOXM1 is a transcription factor overactive across many cancers and long considered hard to drug because it lacks a pocket small molecules can grip. A screen-derived peptide, M1-NP1, disrupted two of FOXM1's protein partnerships and blocked its entry to the nucleus, with anti-cancer activity and a clean early safety profile in mice.
Noise-induced hearing loss has no approved drug, partly because the damage degrades the TrkB receptor that growth-factor therapies rely on. MTFL457, a cell-penetrating peptide that protects TrkB from degradation, preserved hearing and inner-ear synapses in noise-exposed animals in a Molecular Medicine study from a Madrid lab.
LHNVD-110, a single synthetic peptide that strings together conserved fragments of hemagglutinin, neuraminidase, and matrix proteins, raised cross-reactive antibodies in mice that blocked 2009 H1N1, seasonal H3N2, H5N1 bird flu, and an influenza B strain. It is an immunogenicity result, not proof of protection.
A FAERS study found 308 drug-pair signals for pancreatitis in people on GLP-1 and related diabetes drugs. A stricter, period-by-period test cut them to 11 weak ones and zero robust ones. The lesson is about the database, not the drugs.
A study that matched diabetic patients on and off GLP-1 drugs found the drugs really do leave more food in the stomach at endoscopy, 4.7 percent versus 1 percent. No one aspirated, and a standard liquid-diet prep erased the risk.
A real-world analysis of nearly 878,000 people with obstructive sleep apnea tied GLP-1 drugs to fewer strokes, brain bleeds, and deaths. The protective signal weakened every year of follow-up, and the year-one mortality drop is large enough to flag healthy-adherer bias.