Cognitive & Signaling Compounds —
What They're Studied For
A breakdown of the neuropeptides, longevity compounds, and neuromodulators in the Helixera catalog — what each one targets, how researchers use them, and how to choose between them.
At a Glance
The cognitive and longevity category is broader than its name suggests. It spans four distinct research areas that happen to share a common theme — they all act on the brain, nervous system, or the fundamental biology of cellular aging.
Neuroprotective Peptides
Semax and Selank — Russian-developed peptides with clinical use history. Act on BDNF, GABA, and monoamine pathways to protect and enhance CNS function.
Neuromodulatory Peptides
DSIP and VIP — older, more complex compounds affecting sleep architecture, circadian rhythm, HPA axis, and immune signaling simultaneously.
Mitochondrial Biology
NAD+, SS-31, MOTS-c — targeting the energy production machinery that declines with age. Different entry points into the same biological problem.
Aging Hallmarks
Epitalon and FOXO4-DRI — targeting telomere length and cellular senescence directly. The most fundamental interventions in the longevity category.
Semax and Selank are the most practically applicable compounds in this category for cognitive research — both have decades of clinical use in Russia, both have documented human safety profiles, and both are well-characterized mechanistically. They're also complementary opposites: Semax stimulates and Selank calms.
Semax upregulates BDNF — the primary growth factor for neuronal survival and plasticity. Selank modulates GABA-A receptors to reduce anxiety without sedation. Neither mechanism overlaps; they're routinely studied together for this reason.
BDNF upregulation, mild CNS stimulation, stroke recovery and cognitive enhancement. Intranasal or SC. The cognitive activator of the pair.
Full overview →GABA-A modulation, anxiolytic without sedation, immune modulation via tuftsin derivation. The calming, stress-resolving counterpart to Semax.
Full overview →| Use Case | Compound |
|---|---|
| Stroke recovery, BDNF-mediated neuroplasticity, cognitive performance, ADHD/focus research | Semax alone |
| Anxiety/GAD models, PTSD, cognitive performance under stress, immune modulation, withdrawal | Selank alone |
| Balanced cognitive enhancement — activation without anxiety elevation | Semax + Selank |
DSIP and VIP are less commonly understood than Semax/Selank but represent some of the most mechanistically interesting compounds in the category. Both operate across multiple systems simultaneously — they're state modulators rather than single-pathway tools.
| Aspect | DSIP | VIP |
|---|---|---|
| Primary Research Use | Sleep architecture, HPA normalization, withdrawal | Circadian rhythm, autoimmune, ARDS, gut-brain axis |
| Sleep Mechanism | Direct delta oscillation promotion | Circadian synchronization (SCN) — indirect sleep benefit |
| Immune Effects | HPA cortisol normalization | Strong anti-inflammatory — VPAC1/2 on immune cells |
| Clinical Data | Small Eastern European trials | Phase 2 (rheumatoid arthritis, ARDS) |
| Choose When | Sleep architecture is the primary variable | Circadian, inflammation, or gut-brain axis is the focus |
These three compounds address the same underlying problem — age-related mitochondrial decline — from three completely different angles. They're not interchangeable; they're complementary.
| Aspect | NAD+ | SS-31 | MOTS-c |
|---|---|---|---|
| Target | Sirtuin pathway / coenzyme pool | Inner mitochondrial membrane | AMPK / metabolic signaling |
| Primary Effect | Energy metabolism, DNA repair, gene regulation | ETC protection, ROS reduction, cardioprotection | Metabolic adaptation, exercise mimicry |
| Administration | IV, SC, or oral precursors | SC or IV injection | SC injection |
| Clinical Data | Phase 1/2 in multiple indications | Phase 2 (HFpEF, mitochondrial myopathy) | Early clinical emerging |
| Aging Connection | NAD+ depletes with age | ETC dysfunction accumulates with age | Circulating MOTS-c declines with age |
These two target the most upstream causes of biological aging — telomere shortening and cellular senescence. Rather than restoring declining function, they address the cellular mechanisms that drive aging itself.
Slows the aging clock — telomerase activation maintains chromosomal integrity and replicative capacity in dividing cells. 25–34% median lifespan extension in animal models.
Full overview →Removes the damage — selectively kills senescent cells that have accumulated and are actively driving inflammation and tissue dysfunction. Nature 2017 landmark paper.
Full overview →| Research Objective | Best Fit | Why |
|---|---|---|
| Cognitive activation / BDNF | Semax | Direct BDNF upregulation, mild stimulating profile, well-characterized |
| Anxiety / stress without sedation | Selank | GABA-A modulation, clean anxiolytic, no dependence |
| Both cognitive activation + anxiety control | Semax + Selank | Complementary non-overlapping mechanisms |
| Sleep architecture (deep sleep promotion) | DSIP | Specific delta oscillation mechanism, non-sedative |
| Circadian rhythm / autoimmune inflammation | VIP | SCN synchronization + VPAC anti-inflammatory, Phase 2 data |
| Mitochondrial energy restoration | NAD+ | Broadest energy metabolism coverage, most clinical data |
| Cardiac / ETC protection | SS-31 | Inner membrane targeting, Phase 2 cardiac data |
| Metabolic / exercise adaptation | MOTS-c | AMPK activation, exercise mimicry, metabolic flexibility |
| Telomere biology / replicative aging | Epitalon | Only compound with telomerase activation + lifespan data |
| Senescent cell clearance | FOXO4-DRI | Only peptide senolytic with published in vivo data |
All compounds listed are for laboratory research use only. Not for human or veterinary use. Information based on publicly available scientific literature as of 2026. · Helixera Labs LLC © 2026