Asprosin
A glucogenic appetite-stimulating hormone whose antagonism has been proposed as an anti-obesity therapeutic strategy.
Investigational compounds — read carefully
This section covers peptides at the frontier of research. Most entries are preclinical, in early or mid-stage clinical trials, or theoretical. Evidence levels are explicitly marked on every entry.
Nothing on these pages constitutes medical advice, dosing recommendations, or instructions for use. Many of these compounds are not commercially available; some are not legal for human use. Decisions about treatment require a qualified clinician.
At a glance
Identified in 2016 as a fasting-induced hormone that stimulates appetite and hepatic glucose production. Asprosin antagonism is being explored as a novel anti-obesity strategy.
- Class
- Glucogenic / appetite-stimulating hormone
- Sponsor
- Academic research programs (Chopra lab and others)
- Stage
- Preclinical / theoretical
- Lead use case
- Anti-obesity and metabolic disease (via antagonism)
What it is
Asprosin is the C-terminal cleavage product of fibrillin 1 (FBN1), released into circulation primarily during fasting. It acts on the OLFR734 receptor in hepatocytes to stimulate hepatic glucose release, and on AgRP neurons in the hypothalamus to stimulate appetite. Discovered in 2016, asprosin represents a relatively new addition to the appetite-regulation peptide landscape.
Current research status
Asprosin antagonism remains in preclinical / early translational development. Anti-asprosin antibodies and small-molecule antagonists are being explored in academic and biotech programs as anti-obesity candidates with a mechanism distinct from incretin agonism or GDF15 activation.
Mechanistic rationale
The therapeutic concept is asprosin antagonism rather than asprosin agonism — neutralizing endogenous asprosin to reduce hepatic glucose release and appetite stimulation. The mechanism is interesting in part because it represents inhibiting an appetite-stimulating signal rather than activating an appetite-suppressing one — a different conceptual axis than most current obesity pharmacology.
Available evidence
Discovery (Romere et al., Cell 2016) — Asprosin identified as a fasting-induced glucogenic hormone, with elevated levels in obesity and metabolic disease.[1]
Anti-asprosin antibodies in mice — Reduced food intake, weight loss, and improved glycemic parameters in obese rodent models.[2]
Human observational — Circulating asprosin is elevated in obesity, T2D, and metabolic syndrome; the directionality of the association supports the antagonism hypothesis but doesn't establish therapeutic causality.
Why it's interesting
The conceptual symmetry is appealing — most modern obesity drugs activate appetite-suppressing pathways; asprosin antagonism would inhibit an appetite-stimulating pathway. If the therapeutic window can be established and chronic asprosin neutralization produces sustained weight loss without serious off-target effects, it would be a genuinely different therapeutic axis. The mechanism would also potentially work in patients who don't respond to or tolerate the incretin class.
Limitations & risks
Asprosin biology is relatively new — the 10-year research record is modest compared to GLP-1 or even GDF15. Long-term consequences of chronic asprosin antagonism (impaired fasting glucose maintenance, effects on stress responses, off-target effects of FBN1 cleavage products) are not characterized. Translation from rodent antibody work to human therapeutic use is at an earlier stage than essentially all other entries on this page.
Community discussion notes
Limited biohacker-community discussion given the early-stage development. Of considerable academic interest as a representative of the broader 'appetite-stimulating hormone antagonism' therapeutic concept.
The takeaway
Asprosin antagonism is one of the more genuinely novel anti-obesity therapeutic concepts in development. The translation distance is significant and the human evidence base is essentially absent. For readers tracking the field, this represents the long-tail of obesity pharmacology — what's being investigated now that, if it works, would be in clinical use in the 2030s.
References
- Romere C, et al. Asprosin, a Fasting-Induced Glucogenic Protein Hormone. Cell. 2016;165(3):566-579. https://pubmed.ncbi.nlm.nih.gov/27087445/
- Duerrschmid C, et al. Asprosin is a centrally acting orexigenic hormone. Nat Med. 2017;23(12):1444-1453. https://pubmed.ncbi.nlm.nih.gov/29106398/