Humanin 10 mg

Humanin 10 mg research-grade lyophilized peptide powder in a glass vial. Humanin is a naturally occurring 24-amino-acid micropeptide, also known as HN peptide, encoded within the mitochondrial genome and studied in experimental models for its potent cytoprotective and anti-apoptotic properties.

Research Overview

Humanin is a mitochondria-derived micropeptide originally identified in surviving neurons from neurodegeneration models. In research settings it is widely used as a cytoprotective tool to study anti-apoptotic signaling, mitochondrial stress responses and survival pathways in neural, endocrine and metabolic tissues, without implying any therapeutic use.

Primary Research Areas

• Anti-apoptotic & cytoprotective pathways: Experimental assays exploring Humanin-mediated inhibition of apoptosis, including modulation of Bax/Bcl-2 family proteins and downstream caspase activation [1].
• Blood sugar and insulin: infused into the brain of rats, humanin improved whole-body insulin sensitivity, and a potent analogue given into a vein did the same and lowered blood glucose in diabetic Zucker rats. The liver effect disappeared when a hypothalamic signal was blocked [2].
• Plaque in the arteries: mice bred to develop atherosclerosis and fed high cholesterol got daily injections of the humanin analogue HNGF6A for 16 weeks. Plaques in the upper aorta came out smaller and artery lining function was preserved, with no change in cholesterol. The analogue was used, not humanin [3].
• Damage after a heart attack: mice had a coronary artery blocked for 45 minutes; the analogue HNG cut the size of the dead area, best at 2 mg/kg, and one week later pumping function was better than in untreated mice. Again this used HNG, not humanin itself [4].
• Memory in old mice: giving humanin to aged mice improved their performance on memory tests, and it protected human cells in culture. In people, a mitochondrial DNA variant that lowers circulating humanin tracked with faster cognitive ageing in a large national sample [5].
• Cell energy in mitochondrial disease: humanin raised ATP levels in human lymphocytes and in muscle and nerve cell lines, and also in lymphocytes from patients with the mitochondrial disease MELAS. It did this without making cells copy more faulty mitochondrial DNA, which matters in that illness [6].
• Growth hormone lowers it: blood humanin falls with age in mice and people, and giving growth hormone or IGF-1 pushed it down further in both. Long-lived growth-hormone-deficient mice had high levels, so growth-hormone signalling and humanin levels move in opposite directions [7].

References

1. Guo B, Zhai D, Cabezas E, et al. Humanin peptide suppresses apoptosis by interfering with Bax activation. Nature. 2003;423(6938):456-61. PMID 12732850. doi:10.1038/nature01627
2. Muzumdar RH, Huffman DM, Atzmon G, et al. Humanin: a novel central regulator of peripheral insulin action. PLoS One. 2009;4(7):e6334. PMID 19623253. doi:10.1371/journal.pone.0006334
3. Oh YK, Bachar AR, Zacharias DG, et al. Humanin preserves endothelial function and prevents atherosclerotic plaque progression in hypercholesterolemic ApoE deficient mice. Atherosclerosis. 2011;219(1):65-73. PMID 21763658. doi:10.1016/j.atherosclerosis.2011.06.038
4. Muzumdar RH, Huffman DM, Calvert JW, et al. Acute humanin therapy attenuates myocardial ischemia and reperfusion injury in mice. Arterioscler Thromb Vasc Biol. 2010;30(10):1940-8. PMID 20651283. doi:10.1161/ATVBAHA.110.205997
5. Yen K, Wan J, Mehta HH, et al. Humanin Prevents Age-Related Cognitive Decline in Mice and is Associated with Improved Cognitive Age in Humans. Sci Rep. 2018;8(1):14212. PMID 30242290. doi:10.1038/s41598-018-32616-7
6. Kariya S, Hirano M, Furiya Y, et al. Effect of humanin on decreased ATP levels of human lymphocytes harboring A3243G mutant mitochondrial DNA. Neuropeptides. 2005;39(2):97-101. PMID 15752543. doi:10.1016/j.npep.2004.11.004
7. Lee C, Wan J, Miyazaki B, et al. IGF-I regulates the age-dependent signaling peptide humanin. Aging Cell. 2014;13(5):958-61. PMID 25040290. doi:10.1111/acel.12243