Research goal
Immune Support
Covers compounds researched for their effects on immune cell function, inflammatory cytokine modulation, and systemic immune system support in preclinical and clinical settings.
Relevant Compounds
| Compound | Class | Primary mechanism | Commonly reported for | Link |
|---|---|---|---|---|
| TB-500 | Thymosin Beta-4 analogue | Immune cell migration, anti-inflammatory, tissue repair | Immune modulation, recovery, systemic repair | View profile → |
| KPV | α-MSH tripeptide | MC1R/MC3R agonism; anti-inflammatory cytokine suppression; NF-κB inhibition | Anti-inflammation, gut immune crossover | View profile → |
| NAD+ | Dinucleotide coenzyme | PARP/sirtuin activation; supports immune cell energy metabolism; anti-inflammatory via SIRT1 | Immune cell energy, longevity, anti-inflammatory | View profile → |
| Selank | Anxiolytic peptide | Cytokine modulation; IL-6 and interferon regulation; immunomodulatory in research | Cytokine normalisation, anxiolytic, immune balance | View profile → |
Research Context
The thymosin peptide family has been extensively studied for its immunomodulatory properties. TB-500 — the synthetic analogue of Thymosin Beta-4 — is distinct from Thymosin Alpha-1 in both structure and receptor activity, but both belong to a class of thymic peptides implicated in T-cell development and immune regulation. Research has investigated TB-500 for its potential role in reducing pro-inflammatory cytokine release, promoting immune cell migration to sites of injury, and modulating the inflammatory response in a way that may support systemic immune balance rather than broadly suppressing immune activity.
NAD+ depletion has been observed in models of infection and chronic inflammation, driven in part by PARP enzyme overactivation during oxidative stress and DNA damage. SIRT1 — a NAD+-dependent deacetylase — has been studied for its anti-inflammatory role in macrophage polarisation, where it suppresses NF-κB-driven transcription of pro-inflammatory cytokines. Research has investigated NAD+ restoration as a strategy to support immune cell energy metabolism and dampen the chronic inflammatory signalling that characterises many disease states, though clinical translation remains an active area of inquiry.
Selank's immunomodulatory properties have been documented in published Russian-language research focusing on cytokine normalisation — specifically IL-6 and interferon-gamma — in stressed rodent models. This positions Selank as a compound with potential dual relevance: an anxiolytic profile alongside an immune-modulatory one. Its adjunct potential in immune stress contexts has been proposed in the literature, though robust human clinical data remains limited and its primary pharmacological registration is in the context of anxiety and cognitive function.
Compound Notes
TB-500
TB-500 is a synthetic fragment of Thymosin Beta-4, a peptide involved in actin sequestration, cell migration, and immune cell regulation. Research has investigated TB-500 for its potential role in systemic healing and anti-inflammatory signalling. The thymosin family's historical connection to thymic immune function gives TB-500 relevance in immune support contexts beyond its more commonly cited wound-healing and recovery applications. Reported side effects in research and anecdotal accounts include mild injection-site reactions and transient fatigue.
KPV
KPV is the C-terminal tripeptide of alpha-melanocyte-stimulating hormone (α-MSH), retaining the anti-inflammatory activity of the parent molecule with a substantially smaller molecular weight. Research has investigated KPV for its potential role in direct NF-κB inhibition and suppression of IL-1β, TNF-α, and other pro-inflammatory mediators. A notable feature is its reported oral bioavailability — unlike most peptides, KPV appears to reach intestinal tissue intact, making it relevant for gut-immune crossover applications and IBD model research.
NAD+
NAD+ is a dinucleotide coenzyme rather than a peptide, but is frequently included in research contexts alongside peptides due to its role in cellular energy metabolism and its relevance to PARP and sirtuin signalling. Research has investigated its potential role in immune cell function, particularly the SIRT1-mediated anti-inflammatory pathway in macrophages. NAD+ levels decline with age and under conditions of oxidative stress, and the compound's restoration has been studied as a strategy to support both immune competence and resolution of chronic low-grade inflammation.
Selank
Selank is a synthetic heptapeptide developed in Russia, registered as a pharmaceutical anxiolytic and nootropic. Its immunomodulatory properties represent a secondary but well-documented aspect of its pharmacology in preclinical literature. Research has investigated Selank for its potential role in normalising elevated cytokine levels — particularly IL-6 and interferon-gamma — in models of stress-induced immune dysregulation. This dual profile (anxiolytic plus cytokine-modulating) distinguishes Selank from most other compounds in the immune research space.
Commonly Reported Combinations
No widely documented stacks have been established specifically for immune support goals. In anecdotal research community contexts, TB-500 and KPV are sometimes reported together given their complementary anti-inflammatory mechanisms — TB-500 operating via actin/cytoskeletal and thymic pathways, KPV via direct NF-κB suppression. NAD+ is frequently reported alongside other longevity-adjacent compounds rather than as a dedicated immune stack component.
Selank is typically reported as a standalone compound given its anxiolytic primary profile and the limited data on its interaction with other immunomodulatory peptides. Researchers interested in combinations are encouraged to consult individual compound profiles and the related stacks documented under the Recovery and Inflammation goals.
Frequently Asked Questions
How does TB-500 support immune function, given it is primarily associated with healing and recovery?
TB-500's immune-relevant properties are rooted in its origin: Thymosin Beta-4 was first identified in thymic tissue and has documented roles in T-cell maturation and immune cell chemotaxis. Research has investigated TB-500 for its potential role in modulating the inflammatory microenvironment — specifically by downregulating pro-inflammatory cytokines and promoting resolution of acute inflammation. Its healing and immune-modulatory functions appear mechanistically linked through its effects on cell migration and cytokine signalling, rather than being separate profiles.
Is Selank actually an immunomodulator, or is that a secondary effect?
Selank's immunomodulatory properties are documented in peer-reviewed preclinical research and are not merely anecdotal. Studies have measured cytokine changes — particularly in IL-6 and interferon-gamma — in animal models after Selank administration. However, its primary registration and the majority of clinical-adjacent human research has focused on its anxiolytic and nootropic profile. The immunomodulatory effect is best understood as a real but secondary aspect of its pharmacology, likely mediated through its interaction with stress-immune axis signalling.
What does NAD+ depletion during immune stress mean, and what does supplementation research show?
During infection and inflammatory states, PARP enzymes — which are activated by DNA strand breaks caused by oxidative stress — consume large quantities of NAD+. This can deplete intracellular NAD+ levels, impairing the energy metabolism of immune cells and reducing the activity of NAD+-dependent sirtuins like SIRT1, which normally suppress NF-κB-driven inflammation. Research has investigated NAD+ precursor supplementation for its potential role in restoring cellular NAD+ levels in these contexts, with some animal and early human trial data suggesting improved immune cell function and reduced inflammatory markers, though results remain preliminary.
Does route of administration — oral vs subcutaneous — matter for KPV's immune and anti-inflammatory effects?
Yes, and the distinction is pharmacologically significant. KPV's small size (three amino acids) means it is not fully degraded by intestinal proteases, allowing a meaningful portion to reach intestinal epithelial tissue intact via the oral route — a property that most peptides lack. For gut-specific immune and anti-inflammatory effects, the oral route may offer targeted local activity. Subcutaneous administration is expected to produce more systemic distribution. Research has investigated both routes in different contexts, and the oral route has been specifically studied in IBD and colitis models where local mucosal delivery is the intended mechanism.