Peptide Library

Raises brain-derived neurotrophic factor (BDNF) and other trophic signals, modulates dopamine and serotonin turnover, and dampens inflammatory gene expression after brain injury — without ACTH's hormonal effect on cortisol

Appears to modulate GABA-A receptor signalling, slow the breakdown of the brain's enkephalins, and shift serotonin and inflammatory cytokine balance — producing anxiety reduction without sedation in animal and small human studies

Reported to bind hepatocyte growth factor (HGF) and strongly amplify signalling through its receptor c-Met, driving the formation of new synapses in the hippocampus

Claimed to mimic the actions of neurotrophic factors (nerve growth factor, BDNF, CNTF) — supporting neuron survival, reducing inflammation and excitotoxic damage after injury — though no single active component has been identified

Reported to raise BDNF expression in the brain and inhibit the LIF/STAT signalling branch of CNTF, boosting new neuron formation and synaptic protein levels without the growth-factor side effects of CNTF itself

Unclear

Claimed to be neuroprotective and "nootropic" — reducing glutamate toxicity, oxidative stress and inflammation and supporting neuron survival — but the active components are not identified

Broken down in the body to cycloprolylglycine, a dipeptide the brain makes itself; in rodents it raises NGF and BDNF in the hippocampus, protects neurons from oxidative and amyloid-related damage and modulates glutamate signalling

Assumed to be the same as Semax — raises BDNF and NGF signalling in the brain, modulates gene expression after ischaemia and dampens enkephalin breakdown — with the end-caps intended to slow enzymatic degradation

Assumed identical to Selank — modulation of GABA-related signalling, inhibition of enkephalin-degrading enzymes and shifts in immune and inflammatory gene expression — with the caps intended to slow enzymatic breakdown

Stabilises microtubules inside neurons by interacting with microtubule end-binding proteins, which in cells and animals reduces tau tangling, protects synapses and improves survival under stress

Activates orexin receptors OX1R and OX2R on arousal-promoting brain circuits to sustain wakefulness, suppress REM sleep, and raise appetite, reward drive and sympathetic tone

Blocks N-type (CaV2.2) voltage-gated calcium channels on pain-nerve terminals in the spinal cord, stopping release of pain neurotransmitters

Acts at three G-protein-coupled receptors (GalR1–3), mostly inhibitory: it quietens neuronal firing, suppresses insulin release, dampens pain signalling and limits seizure spread

Acts at Y-family receptors: via Y1 and Y5 in the hypothalamus it is the body's most powerful appetite stimulant; via Y1 on blood vessels it constricts; via Y2 it acts as a presynaptic brake, and in the amygdala it promotes stress resilience

Activates the NK1 receptor to transmit pain signals in the spinal cord, trigger neurogenic inflammation in tissue, dilate vessels and drive the vomiting reflex in the brainstem

Acts at the CLR/RAMP1 receptor to produce the most potent microvascular vasodilation known in humans, and to transmit and sensitise trigeminal pain signalling — the central mechanism of migraine

The body's own morphine-like messengers: released by neurons and the pituitary to dampen pain signals, blunt the stress response, shape reward and mood, and regulate gut, breathing and hormone release — acting on the same receptors that…

Does not act on the IGF-1 receptor; appears to normalise synaptic development and dampen neuroinflammation, with effects on microglia, astrocytes and dendritic morphology in Rett models — exact receptor unknown

Enhances cellular zinc uptake and acts on zinc-dependent pathways; activates Nrf2 antioxidant responses; modulates dopamine and appetite signalling in rodents; recently described as a modulator of the chloride channel CLIC1

Block acid-sensing ion channels (ASIC1a and ASIC1b) rather than opioid receptors, producing analgesia in rodents that naloxone does not reverse

Each family blocks or modulates a specific ion channel or receptor with unusual precision — nicotinic receptors (α), voltage-gated sodium channels (μ), calcium channels (ω), noradrenaline transport (χ) — which is why they are the standard…

Selectively blocks small-conductance calcium-activated potassium channels (SK channels, principally SK2/KCa2.2), removing the afterhyperpolarisation that normally limits repetitive firing in neurons and other excitable cells

Crotalphine produces long-lasting analgesia in rodents by activating peripheral opioid receptors (kappa and delta) and engaging cannabinoid signalling; crotamine is a muscle toxin that happens also to be an efficient cell-penetrating and…

Hi1a is a potent and selective inhibitor of acid-sensing ion channel 1a (ASIC1a), the channel that drives cell death when tissue pH falls during loss of blood supply; ProTx-II is a potent inhibitor of the voltage-gated sodium channel…

Activates kappa-opioid receptors on peripheral sensory nerves and immune cells to suppress itch signalling and inflammation, while barely entering the brain, so it avoids the sedation, euphoria and dysphoria of brain-acting opioids