Dihexa

3-NP exposure reduced weight gain, impaired spatial learning and memory, and caused motor dysfunction in rats.; PNB-0408 did not attenuate any of the 3-NP-induced deficits.; PNB-0408 may not be an effective treatment for preventing HD-like symptoms in this preclinical model.; Further research in alternative models or approaches is needed.

Small-molecule cocktail CIP (CHIR99021, IDE1, PD0332991) efficiently induces definitive endoderm via increased endogenous TGF-β/Nodal signaling.; Combination of Vitamin C, Dihexa, and Forskolin (VDF) substitutes growth factors for hepatic specification.; Small-molecule-derived hepatocyte-like cells display mature functional characteristics in vitro and repopulate injured liver in vivo.; The protocol provides a cost-effective platform for large-scale production of functional human hepatic cells for therapy and drug discovery.

Dihexa increased AngIV levels in mouse tissue and restored spatial learning and cognitive function in the Morris water maze test.; Dihexa increased neuronal cells and SYP protein expression while decreasing astrocyte and microglial activation.; Dihexa reduced pro-inflammatory cytokines IL-1 and TNF-α and increased anti-inflammatory cytokine IL-10.; Dihexa activated the PI3K/AKT signaling pathway, and the PI3K inhibitor wortmannin reversed its anti-inflammatory and anti-apoptotic effects.

Ang IV had beneficial effects on passive avoidance and object recognition in 7 of 11 normal animal studies.; In cognitive deficit models, 8 of 9 studies found Ang IV and its analogs improved spatial working memory and passive avoidance.; Ang-(1-7) benefited memory in 2 of 3 studies, and Mas receptor removal reduced fear memory in one study.; Brain RAS peptides are most effective when given intracerebroventricularly close to learning acquisition or retention testing.

Small molecules replace conventional growth factors Wnt3A and activin A for definitive endoderm induction.; CHIR99021 (Wnt agonist) directs primitive streak to definitive endoderm differentiation.; Dimethyl sulfoxide and Dihexa/dexamethasone drive hepatoblast and hepatocyte-like cell maturation.; Protocol is efficient and reproducible for generating HLCs from hPSCs.

Alzheimer's disease involves cognitive impairment and memory deficits, while Parkinson's disease features motor symptoms like bradykinesia and tremor.; The angiotensin IV/AT4 receptor system is linked to learning, memory, and motor functions, though the receptor's identity is debated (IRAP vs. c-Met).; Small molecule AngIV analogs, including Dihexa, were synthesized to be metabolically stable and blood-brain barrier penetrant.; Dihexa shows promise in restoring memory and motor function by promoting new functional synapse formation.

Dihexa at 1 μM provides optimal protection against acute neomycin and gentamicin toxicity.; Protection is not due to reduced aminoglycoside entry into hair cells.; Co-treatment with HGF antagonist 6-AH or inhibitors of Akt, TOR, and MEK attenuates protection.; N-terminal modification of Dihexa reduces its protective efficacy.

What is Dihexa?

**Mechanism of Action** Dihexa (PNB-0408) is a synthetic small peptide derived from angiotensin IV, designed to enhance hepatocyte growth factor (HGF) signaling through its receptor c-Met. Unlike its parent peptide, Dihexa is metabolically stable and crosses the blood-brain barrier. It potentiates HGF/c-Met activity, l

How does Dihexa work?

Angiotensin IV-derived small peptide that potentiates HGF/c-Met signaling to drive synaptogenesis in preclinical cognition models.

What is the research status of Dihexa?

Dihexa is currently classified as preclinical, with 17 research references on record. This is for research purposes only and is not medical advice.

What is the molecular weight of Dihexa?

Dihexa has a molecular weight of approximately 504.7 g/mol (formula C27H44N4O5).