Wholesale Nicotinamide Adenine Dinucleotide NAD+ NADH NAD Powder in Bulk Mots-C Dsip Dihexa Nad+

NAD

Adenosine 5′-(trihydrogen diphosphate),P′→5′-ester with 3-(aminocarbonyl)-1-β-D-ribofuranosylpyridinium,inner salt;Pyridinium,3-carbamoyl-1-β-D-ribofuranosyl-,hydroxide,5′→5′-ester with adenosine 5′-(trihydrogen pyrophosphate),inner salt;Adenosine 5′-(trihydrogen diphosphate),P′→5′-ester with 3-(aminocarbonyl)-1-β-D-ribofuranosylpyridinium hydroxide,inner salt;Codehydrase I;Codehydrogenase I;Coenzyme I;Diphosphopyridine nucleotide;DPN;Cozymase I;NAD;Nadide;Nicotinamide-adenine dinucleotide;Oxidized diphosphopyridine nucleotide;Adenine-nicotinamide dinucleotide;NAD+;Enzopride;β-NAD;β-Diphosphopyridine nucleotide;β-Nicotinamide adenine dinucleotide;β-NAD+;NSC 20272;CO-I;β-Nicotinamide adenine dinucleotide hydrate;30429-30-2;159929-29-0;1083039-67-1;1354693-98-3

53-84-9

C21H27N7O14P2

InChIKey=BAWFJGJZGIEFAR-NNYOXOHSSA-N

663.43

663.109131

200-184-4

757121

DTXSID2045236

C87339

29349990

Other Chemical Drugs

321

-1.29620

White Powder

140-142 °C (decomp)

soluble in water at 50mg/ml

2-8°C

D20 -31.5° (c = 1.2 in water)

226.7 Ų [M+H]+ [CCS Type: DT, Method: single field calibrated with Agilent tune mix (Agilent)]|227.5 Ų [M+H]+ [CCS Type: DT, Method: single field calibrated with ESI Low Concentration Tuning Mix (Agilent)]|222.7 Ų [M+Na]+ [CCS Type: DT, Method: single field calibrated with ESI Low Concentration Tuning Mix (Agilent)]|223.8 Ų [M-H]- [CCS Type: DT, Method: single field calibrated with ESI Low Concentration Tuning Mix (Agilent)]|230.8 Ų [M+Na-2H]- [CCS Type: DT, Method: single field calibrated with ESI Low Concentration Tuning Mix (Agilent)]|227 Ų [M+H]+ [CCS Type: TW, Method: calibrated with polyalanine and drug standards]

Angiotensin IV-derived oligopeptide / HGF-c-Met potentiator

Research compound — Not FDA approved

A synthetic, orally active, blood-brain-barrier-permeable oligopeptide (Hexanoyl-Tyr-Ile-Ahx-NH₂) derived from angiotensin IV. Dihexa binds hepatocyte growth factor (HGF) with high affinity (Kd = 65 pM) and allosterically potentiates HGF activity at its receptor c-Met, promoting dendritic spinogenesis and synaptogenesis. In preclinical models it was reported to be seven orders of magnitude more potent than BDNF at promoting synapse formation. Note: the foundational 2014 paper (McCoy AT, et al. Neurobiol Learn Mem. 2014) was retracted in 2025.

65 pM

Dihexa is an HGF potentiator, not a direct receptor agonist. It does not activate c-Met alone but markedly augments HGF-induced c-Met activation at low nanomolar HGF concentrations. Functional synaptogenic activity was reported at 10⁻¹°–10⁻⁻ M (original data now subject to retraction).

Original report: McCoy AT, et al. Neurobiol Learn Mem. 2014;115:112-120 (retracted 2025). Benoist CC, et al. J Pharmacol Exp Ther. 2014;351(3):628-637.

NCT04488419

PubChem

9WYX65A5C2

Benoist CC, et al. J Pharmacol Exp Ther. 2014 — HGF/c-Met mechanism; McCoy AT, et al. Neurobiol Learn Mem. 2014 — Synaptogenesis data (Retracted 2025); Athira Pharma: Fosgonimeton (prodrug) pipeline status

Dihexa is NOT FDA-approved or EMA-approved as a medicine. It is a research compound only. The foundational 2014 paper describing its synaptogenic potency was retracted in 2025. Its phosphate prodrug fosgonimeton failed a Phase 2/3 Alzheimer’s trial (LIFT-AD, 2024). This listing is for industrial and laboratory research use only. It is not medical advice, a clinical recommendation, or an approved therapy description. Always verify regulatory status, purity, and intended use with the supplier and applicable authorities before purchase or use.