HN, HNG (potent analogue)
Evidence Grade C — Moderate human evidence. 514 published studies, 299 human. 2 registered clinical trials.
Humanin is a peptide encoded in the mitochondrial genome (rather than in nuclear DNA), discovered in 2001 during a search for factors that protect against Alzheimer's-related cell death. It belongs to the emerging field of mitochondrial-derived peptides. No human clinical trials have been conducted. It remains entirely at the preclinical research stage.
514 published studies: 299 human, 135 animal, 112 in-vitro, 80 reviews
Humanin has no marketing authorisation. No human clinical trials have been conducted. The evidence base consists entirely of cell culture and animal studies since its discovery in 2001.
Human observational studies have reported associations between circulating humanin levels and age-related parameters, but observational correlations do not establish therapeutic potential. Like MOTS-c, humanin is of scientific interest within the mitochondrial-derived peptide field but remains at a preclinical stage. No products intended for human use have undergone regulatory review.
Research in cell culture and animal models suggests humanin may interact with multiple signalling pathways including a proposed trimeric receptor complex and anti-apoptotic mechanisms. It was originally identified for its ability to protect neurons from amyloid-beta toxicity in laboratory settings. These observations are entirely preclinical and have not been tested in human trials.
Research in cell culture and animal models suggests humanin may have protective effects against various forms of cellular stress, including amyloid-beta toxicity relevant to Alzheimer's disease. Human observational studies have found correlations between circulating humanin levels and age-related parameters. However, no human clinical trials have been conducted. The evidence consists entirely of preclinical work and observational correlations (which do not establish therapeutic potential). Key concerns include a very short half-life (under 30 minutes), unknown human pharmacology, and a theoretical concern that blocking cell death pathways could promote tumour growth. Modified analogues are under investigation but remain preclinical.
Clinical Value of Plasma Humanin in Acute Kidney Injury
Humanin Isoforms in Cardiac Muscle and Blood Plasma and Major Complications After Cardiac Operation
The information on this page is provided for educational and research reference purposes only. This is not medical advice. Always consult a qualified healthcare professional before making any health-related decisions.
Exenatide was the first GLP-1 receptor agonist approved anywhere, reaching the market as Byetta in April 2005. The once-weekly formulation Bydureon followed in 2012. Clinical trials showed blood sugar reductions (HbA1c) of 1.6–1.9% and modest weight loss of 2–4 kg. The EXSCEL cardiovascular outcomes trial, involving over 14,700 patients, showed a trend toward cardiovascular benefit but narrowly missed statistical significance. While exenatide was groundbreaking as the first in its class, it has been largely overtaken by newer GLP-1 treatments that offer greater efficacy, less frequent dosing, and proven cardiovascular benefits. It remains available and in clinical use, particularly in combination products.
Lixisenatide was marketed as Adlyxin in the US (approved July 2016), though it has since been discontinued in the US market. The ELIXA cardiovascular trial, involving over 6,000 patients, was the first cardiovascular outcomes trial for any GLP-1 medication to report results. It showed a neutral cardiovascular profile — neither harmful nor beneficial — meeting safety requirements but not demonstrating the heart benefits later shown by semaglutide and liraglutide. Lixisenatide found its primary clinical role in combination with basal insulin, marketed as Soliqua (lixisenatide plus insulin glargine). This combination addresses both fasting blood sugar (via insulin) and post-meal spikes (via lixisenatide) in a single daily injection. As a standalone treatment, it has been largely superseded by more potent GLP-1 medications.
Pramlintide is marketed as Symlin (approved March 2005) and remains the only approved amylin-based treatment. It is used alongside mealtime insulin in both type 1 and type 2 diabetes. Clinical trials showed modest blood sugar improvements (HbA1c reductions of 0.2–0.6%) and approximately 2.3 kg of weight loss — less dramatic than GLP-1 treatments but meaningful as an add-on therapy. Symlin carries a boxed warning for severe hypoglycaemia, particularly when combined with insulin, and requires careful dose adjustment. Practical uptake has been limited by the need for separate injections at each meal alongside existing insulin injections. Despite its modest clinical impact, pramlintide remains the only medication that addresses the amylin deficiency in diabetes, filling a distinct biological role that GLP-1 treatments do not cover.
