Research news · 4 min read
Peptide research roundup: 26 October 2026

This is the second edition of our weekly roundup of new peptide research. It covers papers added to PubMed between 20 and 26 October 2026 on the compounds in our catalogue, with what each study measured, in what model, and where it stops. The first edition, covering mid-August to 20 October, is here.
It is a summary of published research, not medical advice and not a suggestion to use any compound on people or animals.
Retatrutide: the sleep apnoea trials in full
Last week's roundup covered the main TRIUMPH-1 and TRIUMPH-2 papers. This week, The New England Journal of Medicine (21 October 2026) published the two sleep apnoea trials nested inside them as a paper of their own, by Grunstein and colleagues. Both were funded by Eli Lilly, and retatrutide is not approved for any use.
- Design: two phase 3, double-blind, placebo-controlled trials in adults with moderate-to-severe obstructive sleep apnoea and a body-mass index of at least 27. TRIUMPH-1-OSA enrolled 243 people without type 2 diabetes and TRIUMPH-2-OSA enrolled 448 people with it. Each was randomised to one of three retatrutide dose levels or placebo for 80 weeks.
- The primary outcome was the change in the apnoea-hypopnoea index (AHI), the average number of breathing pauses and shallow-breathing events per hour of sleep. At the start it averaged 58.6 and 55.9 events per hour in the two trials.
- In TRIUMPH-1-OSA, the AHI fell by 22.9 to 34.3 events per hour across the retatrutide groups, against 9.9 with placebo. These figures also appeared in last week's TRIUMPH-1 paper.
- New this week is TRIUMPH-2-OSA, in people with type 2 diabetes: the AHI fell by 19.2 to 25.4 events per hour, against 10.3 with placebo.
- Body weight changed by −12.5 to −22.2% in TRIUMPH-1-OSA and −12.1 to −18.5% in TRIUMPH-2-OSA, against −4.8% and −5.6% with placebo. The most common adverse events were gastrointestinal.
Background: What is retatrutide?
Tirzepatide: a mouse liver study and a large records study
Two papers this week look at tirzepatide from very different angles.
- Liver proteins in obese mice (Journal of Proteome Research, 2 October 2026, added to PubMed this week). Patel and colleagues fed male mice a high-fat diet for 18 weeks, then gave semaglutide, tirzepatide or a vehicle control for 4 weeks. Tirzepatide reduced body weight by 24.6% and fat mass by 30.3%. Using targeted mass spectrometry, confirmed by western blotting, the authors found that both compounds lowered two liver proteins that bring fatty acids in for burning, CD36 and CPT1A, while leaving fat-building enzymes and glucose-handling proteins unchanged. Because the two compounds produced overlapping liver signatures, the authors suggest that GLP-1 receptor activation is enough for the core liver response, with GIP activity mainly acting elsewhere in the body.
- Health records in COPD (Frontiers in Pharmacology, 2026). Hsu and colleagues used the TriNetX records network to compare adults with both chronic obstructive pulmonary disease and type 2 diabetes who were prescribed tirzepatide with matched groups prescribed other glucose-lowering drugs, with 4,684 to 6,727 people in each matched group. Compared with SGLT2 and DPP-4 inhibitors, tirzepatide use was associated with fewer COPD flare-ups (hazard ratios 0.73 and 0.72) and lower all-cause mortality. Against other GLP-1 agonists, the outcomes were similar apart from lower mortality. This is an observational study: it shows associations, not cause and effect, and the median follow-up was about 8 months for tirzepatide against 12 months for the comparison drugs. The authors call for randomised trials to confirm it.
Background: What is tirzepatide? and Retatrutide vs tirzepatide
MOTS-c: a diabetic kidney model
In Biochemical Pharmacology (23 October 2026), Wang and colleagues studied MOTS-c in db/db mice, a standard diabetic mouse strain, and in HK-2 human kidney tubule cells. MOTS-c was associated with lower urine albumin, less tubular injury, less fat build-up in the kidney and fewer markers of cell ageing (senescence). The authors trace it to lower levels of LARS1, a protein that holds back lipophagy, the process cells use to break down stored fat droplets. Raising LARS1 in the cells, or blocking autophagy in the mice, largely removed the effect. All of this is in animals and cells. Background: What is MOTS-c?
Nothing new this week
We found no new primary studies this week on BPC-157, TB-500 or thymosin β4, GHK-Cu, KPV, tesamorelin, Semax, Selank, ipamorelin, CJC-1295, IGF-1 LR3 or NAD+.
Compounds in this roundup
Certificates of analysis for each batch are on each product page once they are on file, and in the certificate library.
- Retatrutide: the GIP, GLP-1 and glucagon receptor triple agonist.
- Tirzepatide: the GIP and GLP-1 receptor dual agonist.
- MOTS-c, 10 mg: the 16-residue peptide encoded in the 12S rRNA gene.
Sources
- Grunstein R.R. et al. Retatrutide Once Weekly for Treatment of Obstructive Sleep Apnea. The New England Journal of Medicine, 2026
- Patel D. et al. Semaglutide and Tirzepatide Suppress Hepatic Fatty Acid Uptake and Fatty Acid β-Oxidation in High-Fat Diet-Induced Obesity Mice. Journal of Proteome Research, 2026
- Hsu W.H. et al. Tirzepatide versus other glucose-lowering therapies and risk of COPD exacerbations in patients with comorbid type 2 diabetes: a retrospective cohort study. Frontiers in Pharmacology, 2026
- Wang J. et al. Mots-c attenuates diabetic nephropathy by downregulating LARS1 to promote lipophagy and suppress tubular senescence. Biochemical Pharmacology, 2026
For laboratory research use only. Nothing in this article is medical advice or a suggestion to use any compound on people or animals.
For laboratory research use only. Not for human or veterinary use. Nothing here is medical advice.