Phoenixin-14 TFA  (Synonyms: PNX-14 TFA)

Phoenixin-14 (PNX-14) TFA is an endogenous neuropeptide with multiple biological activities, and serves as the endogenous ligand of GPR173. Phoenixin-14 TFA reduces ROS production by inhibiting the HMGB1/TLR4/MyD88/NF-κB signaling axis, thereby exerting antioxidant and mitochondrial protective effects. Phoenixin-14 TFA inhibits FOXO3 phosphorylation by upregulating SIRT3 expression, suppresses apoptosis, and improves myocardial systolic/diastolic function. Phoenixin-14 TFA resists ferroptosis by activating the ATF4/SLC7A11/GPX4 axis; it activates ERK1/2 phosphorylation via GPR173. Phoenixin-14 TFA can be used in researches on neuroprotection, diabetes, cardiomyopathy, reproductive protection and so on^[1][2][3][4].

Phoenixin-14 (1-1000 nM; 24 h) TFA directly stimulates progesterone and estradiol secretion by porcine luteal cells on days 10-12 of the estrous cycle via upregulating the expression of steroidogenic enzymes; whereas combined treatment with luteinizing hormone (LH) (HY-P2293) attenuates progesterone secretion and the expression of steroidogenic enzymes^[1].
Phoenixin-14 (1-1000 nM; 24 h) TFA regulates prostaglandin secretion in porcine luteal cells on days 10-12 of the estrous cycle by increasing PGE₂ levels, decreasing PGF₂α levels, and downregulating prostaglandin receptor expression^[1].
Phoenixin-14 (1-1000 nM; 24 h) TFA upregulates the expression of GPR173 protein in porcine luteal cells on days 10-12 of the estrous cycle, and activates multiple kinase signaling pathways, including enhancing the phosphorylation of ERK1/2 and AKT, reducing the phosphorylation of PKA, and exerting time-dependent mixed effects on the phosphorylation of AMPKα and PKC^[1].
The luteotropic effect of Phoenixin-14 (10 nM; 24 h) TFA on steroid and prostaglandin secretion in porcine luteal cells on days 10-12 of the estrous cycle is mediated via the GPR173 and ERK1/2 signaling pathways, independent of the PKA pathway^[1].
Phoenixin-14 (50-100 nM; 24 h) TFA dose-dependently alleviates cisplatin-induced injury, oxidative stress and ferroptosis in KGN cells by restoring the ATF4/SLC7A11/GPX4 axis^[2].
Phoenixin-14 (5-10 nM; 30 h) TFA dose-dependently inhibits the OGD/R-induced increases in mRNA and protein levels of TNF-α, IL-1β and IL-6 in BV2 microglia^[4].
Phoenixin-14 (5-10 nM; 30 h) TFA dose-dependently reduces OGD/R-induced ROS production and restores depleted GSH levels in BV2 microglia^[4].
Phoenixin-14 (5-10 nM; 30 h) TFA dose-dependently reverses the OGD/R-induced decrease in mitochondrial membrane potential in BV2 microglia, and the 10 nM dose almost completely abolishes this decrease^[4].
Phoenixin-14 (5-10 nM; 30 h) TFA dose-dependently attenuates the decrease in viability of BV2 microglia induced by OGD/R, with the 10 nM dose almost maintaining the baseline cell viability^[4].
Phoenixin-14 (5-10 nM; 30 h) TFA dose-dependently inhibits the OGD/R-induced increase in HMGB1 protein level in BV2 microglia^[4].
Phoenixin-14 (5-10 nM; 30 h) TFA dose-dependently inhibits the OGD/R-induced increases in mRNA and protein levels of TLR4 and MyD88 in BV2 microglia^[4].
Phoenixin-14 (5-10 nM; 30 h) TFA inhibits OGD/R-induced nuclear translocation of NF-κB p65 and activation of NF-κB luciferase activity in BV2 microglial cells in a dose-dependent manner^[4].
Phoenixin-14 (10 nM; 30 h) TFA exerts a protective anti-inflammatory effect against OGD/R injury in BV2 microglia, and this effect depends on the GPR173 signaling pathway^[4].
Phoenixin-14 (100 nM; 24 h) TFA reverses the decreases in viability, angiogenesis and migration capacity of human umbilical vein endothelial cells induced by conditioned media from iSMC and SMC, and also reverses the apoptosis induced by these media^[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Phoenixin-14 (50 μg/kg; i.p.; daily; 3 days) TFA improves body and ovary weights, restores ovarian follicle development, and inhibits ferroptosis via the ATF4/SLC7A11/GPX4 axis to alleviate cisplatin-induced premature ovarian failure in female Sprague-Dawley rats^[2].
Phoenixin-14 (100 mg/kg; i.p.; daily; 2 months) TFA protects against streptozotocin-induced diabetic cardiomyopathy in C57BL/6 mice by improving cardiac function, reducing myocardial injury, ameliorating cardiac hypertrophy, mitigating oxidative stress and inflammation, and restoring SIRT3/FOXO3 signaling, with no observed effects on normal mice^[3].
Phoenixin-14 (15 nmol; i.c.v.; single dose; 1 h prior to MCAO) TFA reduces ischemia/reperfusion-induced brain infarct volume to just under 20% and suppresses microglial activation in a rat MCAO ischemic stroke model^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

1583.78 (free base)

C₇₅H₁₁₀N₁₈O₂₀.xC₂HF₃O₂

Asp-Val-Gln-Pro-Pro-Gly-Leu-Lys-Val-Trp-Ser-Asp-Pro-Phe-NH2

DVQPPGLKVWSDPF-NH2

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Mlyczyńska E, et al. Phoenixin-14 as a novel direct regulator of porcine luteal cell functions†. Biol Reprod. 2024;110(1):154-168.

  [2]. Wu R, et al. Phoenixin-14 Alleviates Premature Ovarian Failure by Inhibiting Ferroptosis Through SLC7A11/GPX4. Drug Dev Res. 2025;86(5):e70110.

  [3]. Yao B, et al. Phoenixin-14 protects cardiac damages in a streptozotocin-induced diabetes mice model through SIRT3. Arch Physiol Biochem. 2024;130(1):110-118.

  [4]. Ma H, et al. Phoenixin 14 inhibits ischemia/reperfusion-induced cytotoxicity in microglia. Arch Biochem Biophys. 2020 Aug 15;689:108411.
   [Content Brief]

  [5]. Ling C, et al. Phoenixin-14 alleviates inflammatory smooth muscle cell-induced endothelial cell dysfunction in vitro. Cytokine. 2022;157:155973.