Peptide Library
Boosts the maturation and function of T cells, dendritic cells and natural killer cells, largely by acting on Toll-like receptors (TLR2 and TLR9), and helps rebalance an over- or under-active immune response
Proposed to restore T-cell maturation and balance immune function, and — per the bioregulator hypothesis — to influence gene expression in thymus and immune cells; mechanism is poorly characterised by Western standards
Proposed to activate telomerase, normalise melatonin rhythm and act as a "pineal bioregulator" that resets age-related changes in gene expression; the telomerase claim rests on cell-culture data
Proposed to enter neurons and alter gene expression (e.g. of proteins involved in cell division and ageing), reduce oxidative stress and protect neurons from hypoxia and excitotoxicity; mechanism is from cell culture and molecular modelling
Protects cells from stress-induced death by blocking the pro-death protein Bax, binding IGFBP-3, and signalling through cell-surface receptors (FPRL1/FPR2 and a CNTFR/WSX-1/gp130 complex) — shown in cells and rodents
Acts as a metabolic stress signal: activates AMPK in muscle, alters the folate–methionine cycle, and under stress moves into the nucleus to switch on stress-response genes
Binds cardiolipin in the inner mitochondrial membrane, stabilising cristae structure and the electron-transport chain so cells make more ATP and leak fewer free radicals
Breaks the grip between FOXO4 and p53 inside senescent ("zombie") cells, freeing p53 to trigger their self-destruction while sparing normal cells
Donates electrons to neutralise reactive oxygen species and detoxify compounds via glutathione-S-transferases; recycled by glutathione reductase
Proposed to enter cells and alter gene expression in immune and other tissues, nudging ageing cells toward a more active state; mechanism rests on cell-culture and modelling work
Proposed to alter gene activity in liver and immune cells by loosening condensed chromatin; based on cell-culture work from one group
Reported to normalise T-cell numbers and function and to inhibit angiogenesis; the molecular target is not established
A genuine thymic hormone that helps T cells mature and keeps immune signalling balanced; in rodents it also damps inflammation and pain
Claimed to protect and stimulate retinal pigment epithelium and photoreceptors and to improve retinal metabolism; active components not identified
Proposed to stimulate cell activity in testicular and pituitary tissue and restore hormone output in ageing males via gene-expression effects; evidence is in vitro and from one group
Proposed to enter cells, bind DNA at gene-promoter regions and nudge expression of genes involved in cardiomyocyte survival and fibroblast activity — shown only in cell and rodent work from one group
Proposed to regulate gene expression in bronchial and gastric epithelium — including antioxidant and anti-inflammatory genes — via DNA binding; cell and rodent data from one group
Proposed to bind DNA in bronchial epithelial cells and alter expression of genes for proliferation, differentiation and mucin/antioxidant function; shown in culture and rodents by one group
Proposed to regulate gene expression in vascular endothelium and smooth muscle — and, in later work, in neurons — through DNA binding; cell and rodent evidence from one group
Proposed to regulate gene expression in hepatocytes and gut epithelium — proliferation, antioxidant and detoxification genes — via DNA binding; evidence from one group, cell and rodent
Proposed to enter cells and bind DNA/histones to shift gene expression toward neuronal survival and repair, and to support regeneration of injured nerves — shown only in rodents and cell culture by one group
Proposed, by analogy with the rest of the family, to enter bladder-wall cells and modulate gene expression toward normal tissue function and repair; no published experiment demonstrates this for Vesilute itself
Competitively blocks the bradykinin B2 receptor so the excess bradykinin produced in an HAE attack cannot make blood vessels leak
Binds cyclophilin inside T cells; the complex blocks calcineurin, so T cells cannot switch on IL-2 and other activation genes
Reproduces the active site of thymopoietin, promoting maturation and regulation of T lymphocytes — a "two-way" immune modulator
Thought to shift the immune response away from attacking myelin — inducing regulatory/anti-inflammatory T cells and acting as a decoy resembling myelin basic protein
Binds complement protein C3 and its fragment C3b, blocking all three complement activation pathways at their convergence point
Binds complement C5 at two sites, preventing its cleavage into C5a and C5b and so stopping formation of the membrane-attack complex that damages the neuromuscular junction
Delivers only the T-cell-recognised parts of an allergen, deliberately too short to be cross-linked by IgE on mast cells, so the immune system can be re-educated toward tolerance without triggering an allergic reaction
Delivers the autoantigen epitope under conditions designed to induce regulatory rather than effector T cells, aiming to switch off the specific autoimmune attack while leaving the rest of the immune system intact
Looking for MK-677, NAD+ or rapamycin? They aren't peptides — see Not a peptide, but often discussed with them.