NAD+

NAD⁺ (Nicotinamide Adenine Dinucleotide) is a critical coenzyme present in all living cells and essential for cellular energy metabolism. NAD⁺ functions as a redox carrier in mitochondrial ATP production and serves as a substrate for sirtuins, PARPs, and other NAD-dependent enzymes involved in DNA repair, metabolic regulation, and cellular stress response. In research settings, NAD⁺ is studied for its role in mitochondrial function, aging biology, genomic stability, and metabolic homeostasis.

1000MG | Physician Use

$117.30

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Research Profile

At a Glance

Type: Synthetic EPO-Derived Peptide (Helix-B Domain)
Also Known As: Cibinetide
Sequence: QEQLERALNSS (11 amino acids)
Molecular Weight: 1,257.3 Da
Primary Target: Innate Repair Receptor (EPOR/CD131 heterodimer)
Research Focus: Neuroprotection, nerve regeneration, anti-inflammatory, pain modulation
Regulatory Status: RUO (Research Use Only); FDA Orphan Drug Designation for sarcoidosis-induced neuropathic pain
Categories: Neuropathy Research; Inflammation Research; Tissue Repair; Metabolic Research

What Research Shows

Activates the Innate Repair Receptor (IRR) to reduce key inflammatory cytokines (TNF-α, IL-1β, IL-6) and suppress NF-κB signaling, supporting investigation into tissue protection and anti-inflammatory mechanisms.
Demonstrates neuroprotective effects in preclinical and human studies, including improvements in corneal nerve fiber density and reductions in neuropathic pain symptoms associated with small-fiber nerve damage.
Protects endothelial and microvascular systems in experimental models, reducing vascular leakage, supporting nitric-oxide–related vasodilation, and improving microcirculatory function after inflammatory or ischemic stress.
Enhances cellular survival and reduces tissue injury during ischemia/reperfusion events, indicating a potential role in research focused on organ and tissue recovery.
Shows exploratory benefits in autoimmune and systemic inflammatory conditions, with early studies noting reductions in inflammatory markers and symptom burden, though findings remain preliminary.

Mechanistic Notes

ARA-290’s activity centers on selective Innate Repair Receptor activation:

Core Mechanisms

Binds to the Innate Repair Receptor (IRR) – a heterodimer of EPOR and CD131 (β-common receptor)
Does NOT activate the EPOR homodimer responsible for erythropoiesis
Triggers anti-apoptotic and pro-survival signaling cascades
Reduces pro-inflammatory cytokines (TNF-α, IL-6)
Shifts immune cells toward repair phenotypes

Why ARA-290 Is Distinct from EPO

No stimulation of red blood cell production (no hematocrit increase)
No cardiovascular risks associated with EPO therapy (thrombosis, hypertension)
Selectively targets tissue repair pathways upregulated during injury
Well-tolerated safety profile in Phase II clinical trials

Downstream Effects Observed in Research

Promotes neurite outgrowth and nerve fiber regeneration
Enhances angiogenesis and microvascular function
Reduces oxidative stress and ischemic damage
Blocks TRPV1 channels for direct pain modulation
Suppresses spinal microglia response in neuropathic pain models

What Remains Unknown

Optimal dosing protocols for different research applications
Long-term durability of nerve regeneration effects
Full scope of IRR-mediated signaling pathways
Comparative efficacy across different neuropathy models
Potential synergistic effects with other neuroprotective compounds
All findings are research-only and preliminary.

Scientific References (Peer-Reviewed Only)

Brines M, Dunne AN, van Velzen M, et al. Mol Med. 2015.
https://pmc.ncbi.nlm.nih.gov/articles/PMC4365069/

Dahan A, Dunne A, Swartjes M, et al. Mol Med. 2013.
https://pmc.ncbi.nlm.nih.gov/articles/PMC3928087/

Heij L, Niesters M, Swartjes M, et al. Mol Med. 2012.
https://pmc.ncbi.nlm.nih.gov/articles/PMC3883966/

Dahan A, Brines M, et al. Expert Opin Investig Drugs. 2013.
https://www.tandfonline.com/doi/full/10.1517/21678707.2013.719289

Pulman KG, Smith M, et al. Peptides. 2016.
https://pubmed.ncbi.nlm.nih.gov/26774587/

Brines M, Cerami A. Mol Med. 2012.
https://pubmed.ncbi.nlm.nih.gov/22231730/

Certificate of Analysis

ARA-290 COA