Phoenixin-20 TFA
Phoenixin-20 TFA (PNX-20 TFA) is a neuropeptide that activates GPR173. Phoenixin-20 TFA inhibits LPS-induced TLR-4/MyD88/NF-κB signaling, pro-inflammatory cytokines, adhesion molecules, MMPs, and cytotoxicity. Phoenixin-20 TFA increases SIRT1 and inhibits NLRP3/ASC/caspase-1, oxidative stress, and IL-1β/IL-18. Phoenixin-20 TFA alleviates ox-LDL-induced endothelial dysfunction, monocyte adhesion, adhesion molecules, cytokines, NADPH oxidase/NOX-4, and ROS. Phoenixin-20 TFA promotes GPR173/STAT6-mediated anti-inflammatory polarization of microglia and neuroprotection. Phoenixin-20 TFA can be used in research on dental pulp infection, pulmonary arterial hypertension, atherosclerosis, neuroinflammation, anxiety, and neurodegenerative diseases.
Nos produits utilisent uniquement pour la recherche. Nous ne vendons pas aux patients.
- Formule: C101H153N25O29.xC2HF3O2
- Masse moléculaire:2181.45 (free base)
-
Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
Other In-stock Forms of Phoenixin-20 TFA
-
Activité biologique
-
Chemical Information
- Protocole
- Pureté et documentation
- Références
-
Help & FAQs
Voir tous les produits spécifiques à Isoform Caspase
More
Activité biologique
Description
|
GPR173 |
TLR4 |
NF-κB |
MyD88 |
SIRT1 |
NLRP3 |
Caspase-1 |
ASC |
IL-1β |
IL-18 |
NOX4 |
STAT6 |
In Vitro
Phoenixin-20 (20 nM; 24 h) TFA inhibition of NLRP3/ASC in hypoxia-treated human PMECs is mediated by SIRT1[2].
Phoenixin-20 (20 nM; 24 h) TFA inhibits LPS-induced NLRP3 expression in BV2 microglial cells, an effect that depends on SIRT1 activity and can be abolished by Nicotinamide (HY-B0150) (1 mM)[6].
Phoenixin-20 (10-20 nM) TFA reduces inflammatory cytokine secretion in hypoxia-treated human PMECs[2].
Phoenixin-20 (10-20 nM; 24 h) TFA inhibits LPS-induced IL-1β and IL-18 secretion in BV2 microglial cells[6].
Phoenixin-20 (20 nM; 24 h) TFA inhibits LPS-induced IL-1β and IL-18 production in BV2 microglia, a process that requires SIRT1 activity, and this effect can be abolished by Nicotinamide (1 mM)[6].
Phoenixin-20 (15-30 nM; 24 h) TFA inhibits LPS-induced NF-κB activation by suppressing p65 nuclear translocation and NF-κB reporter gene activity in hDPCs[1].
Phoenixin-20 (15-30 nM; 24 h) TFA lost its inhibitory effect on LPS-induced MMP-2, MMP-9, and NF-κB activation in GPR173-silenced hDPCs, indicating that this effect requires GPR173[1].
Phoenixin-20 TFA-induced M2 polarization of BV2 microglia depends on GPR173, as GPR173 knockdown abolishes the induced expression of M2 markers[7].
Phoenixin-20 (10-20 nM; 24 h) TFA inhibits LPS-induced NOX-4 and TxNIP mRNA and restores SIRT1 mRNA in BV2 microglial cells[6].
Phoenixin-20 (10-20 nM; 24 h) TFA inhibits LPS-induced protein expression of NOX-4, TxNIP, NLRP3, ASC, and cleaved caspase-1 (P10) and restores SIRT1 protein in BV2 microglial cells[6].
Phoenixin-20 (10-20 nM; 24 h) TFA dose-dependently inhibits LPS-induced intracellular ROS production in BV2 microglial cells[6].
Phoenixin-20 (100 nM; 1.5 h) TFA increases the glycolysis-related ATP production rate in zebrafish liver (ZFL) cells without altering the total ATP production rate[8].
Phoenixin-20 (5-20 nM; 48 h) TFA activates CREB, and inhibition of CREB by H89 (10 μM) prevents its effects on mitochondrial regulators and biogenesis in M17 cells[10].
Phoenixin-20 (15-30 nM; 24 h) TFA inhibits LPS-induced MMP-2 and MMP-9 expression in hDPCs[1].
Phoenixin-20 (1-100 nM; 1-24 h) TFA upregulated vitellogenin, esr2a, esr2b, and shbg mRNA expression in zebrafish liver (ZFL) cells, supporting a vitellogenic effect[9].
Phoenixin-20 (10-100 ng/mL; 24 h) TFA stimulates oocyte maturation in zebrafish stage III follicles by increasing germinal vesicle breakdown[9].
Phoenixin-20 (5-20 nM; 48 h) TFA dose-dependently induces PGC-1α mRNA and protein in M17 cells[10].
Phoenixin-20 (5-20 nM; 48 h) TFA dose-dependently induces NRF-1 and TFAM mRNA and protein in M17 cells[10].
Phoenixin-20 (48 h) TFA enhances mitochondrial respiration rate and ATP production in M17 cells[10].
Phoenixin-20 TFA increases GPR173 mRNA approximately threefold and GPR173 protein approximately 2.5-fold in M17 cells[10].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Cell Line:human dental pulp cells (hDPCs)
-
Concentration:15 and 30 nM
-
Incubation Time:24 h (with 20 μg/mL LPS)
-
Result:At 15 and 30 nM, decreased LPS-induced LDH release in a dose-responsive manner.
-
Cell Line:Human pulmonary microvascular endothelial cells (PMECs)
-
Concentration:20 nM
-
Incubation Time:24 h
-
Result:Hypoxia-induced increases in NLRP3 and ASC were repressed at 20 nM, but this repression was reversed by SIRT1 knockdown.
-
Cell Line:BV2 microglial cells
-
Concentration:10 nM and 20 nM
-
Incubation Time:24 h
-
Result:LPS-induced NOX-4 mRNA was dose-responsively suppressed.
LPS-induced TxNIP mRNA was dose-responsively inhibited.
LPS-induced repression of SIRT1 mRNA was robustly ameliorated.
20 nM produced the greatest inhibition where noted.
-
Cell Line:BV2 microglial cells
-
Concentration:10 nM and 20 nM
-
Incubation Time:24 h
-
Result:LPS-induced NOX-4 protein was suppressed.
LPS-induced TxNIP protein was dose-responsively inhibited.
LPS-induced NLRP3, ASC, and cleaved caspase-1 (P10) were significantly suppressed.
20 nM showed the greatest inhibitory effect.
LPS-induced repression of SIRT1 protein was robustly ameliorated.
-
Cell Line:BV2 microglial cells
-
Concentration:10 nM and 20 nM
-
Incubation Time:24 h
-
Result:LPS-induced production of IL-1β and IL-18 was inhibited.
-
Cell Line:BV2 microglial cells
-
Concentration:20 nM (Phoenixin-20); 1 μg/mL (LPS); 1 mM (nicotinamide)
-
Incubation Time:24 h
-
Result:SIRT1 activation blockage by Nicotinamide completely abolished the inhibitory effect on LPS-induced NLRP3 expression.
-
Cell Line:BV2 microglial cells
-
Concentration:20 nM (Phoenixin-20); 1 μg/mL (LPS); 1 mM (nicotinamide)
-
Incubation Time:24 h
-
Result:SIRT1 activation blockage completely abolished the inhibitory effect on LPS-induced IL-1β and IL-18 production.
-
Cell Line:BV2 murine microglial cells
-
Concentration:20 nM (with 10 ng/mL IL-4)
-
Incubation Time:6 h
-
Result:Increased Fizz1, Arg-1, YM1, and IL-10 expression.
Increased p-STAT6 levels.
In Vivo
Phoenixin-20 (4 mg/kg; s.c.) TFA elicits repetitive scratching behavior in male Swiss-Webster mice with pruritus[5].
Phoenixin-20 (2 µg per mouse; i.c.v. into the lateral cerebral ventricle; consecutive injection before and after induction; initiated 24 h before MCAO and maintained during the experiment) TFA reduces brain infarction and neurological deficit and promotes an M2-like microglial marker profile in C57BL/6 MCAO mice[7].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Animal Model:male, 7-9 weeks[2]
-
Dosage:100 ng/g body weight
-
Administration:injected; daily; 28 days
-
Result:RVSP was maintained around 20 mmHg.
mPAP was 19.17 mmHg.
RV/LV+S was 0.27.
W% was 22.16%.
TNF-α was 15.02 pg/mL.
IL-6 was around 37 pg/mL.
MCP-1 was 11.96 pg/mL.
MDA was 1.09 nmol/mg protein.
SOD activity was 67.3 U/mg protein.
-
Animal Model:male, 7-9 weeks[2]
-
Dosage:100 ng/g body weight
-
Administration:injected; daily; 28 days
-
Result:RVSP was 26.53 mmHg.
mPAP was 25.24 mmHg.
RV/LV+S was 0.31.
W% was 30.33%.
TNF-α was 22.96 pg/mL.
IL-6 was 45.32 pg/mL.
MCP-1 was 14.25 pg/mL.
MDA was 1.32 nmol/mg protein.
SOD activity was 56.4 U/mg protein.
-
Animal Model:Swiss-Webster (male, 20-25 g)[5]
-
Dosage:4 mg/kg
-
Administration:s.c.; to nape of the neck; 30 min
-
Result:Evoked 57 scratching bouts (n = 7) across 30 min.
Latency was 3-5 min and duration was 10-15 min.
-
Animal Model:C57BL/6 (male, 8-12 weeks, 25-30 g)[7]
-
Dosage:2 µg per mouse (25-30 g body weight)
-
Administration:i.c.v. into the lateral cerebral ventricle; consecutive injection before and after induction; initiated 24 h before MCAO and maintained during the experiment
-
Result:Brain infarction volume was approximately 17%, compared with about 33% in placebo MCAO mice.
Neurological deficit score averaged 17%, compared with about 33% in placebo MCAO mice.
After three days, peri-infarct brain tissue had lower CD11b, CD86, iNOS, TNF-α, and IL-6 expression and higher Fizz1, Arg-1, YM1, and IL-10 expression than placebo MCAO mice.
- Phagocytosis Functional Assay
- Research Protocol for Infectious Diseases
- LPS-Induced Endotoxemia/Systemic Inflammation
- Cell Cytotoxicity Assay
- Mammalian live/dead viability and cytotoxicity staining
- ROS/oxidative-stress fluorescent staining
- Apoptosis Solutions
- Research Protocol for Cardiovascular Diseases
- Research Protocol for Inflammation-related Diseases
- Research Protocol for Neurological Diseases
- Cell Viability Determination by MTT Colorimetric Assay
- Pyroptosis Solutions
Chemical Information
-
Masse moléculaire 2181.45 (free base)
-
Formule C101H153N25O29.xC2HF3O2
-
Synonyms
PNX-20 TFA
-
Sequence
Ala-Gly-Ile-Val-Gln-Glu-Asp-Val-Gln-Pro-Pro-Gly-Leu-Lys-Val-Trp-Ser-Asp-Pro-Phe-NH2
-
Sequence Shortening
AGIVQEDVQPPGLKVWSDPF-NH2
-
Livraison
Room temperature in continental US; may vary elsewhere.
-
Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureté et documentation
Références
[5]. Cowan A, et al. Phoenixin: A candidate pruritogen in the mouse. Neuroscience. 2015 Dec 03;310:541-8.
[9]. Rajeswari JJ, et al. Phoenixin-20 Stimulates mRNAs Encoding Hypothalamo-Pituitary-Gonadal Hormones, is Pro-Vitellogenic, and Promotes Oocyte Maturation in Zebrafish. Scientific reports. 2020 Apr 14;10(1):6264. [Content Brief]
[10]. Yang Y, et al. Phoenixin 20 promotes neuronal mitochondrial biogenesis via CREB-PGC-1α pathway. Journal of molecular histology. 2020 Apr;51(2):173-181. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Phoenixin-20 TFA Related Classifications
HY-P5763A Related Classifications
Powered by Bioz
Keywords
- Phoenixin-20
- PNX-20
- Phoenixin20
- Phoenixin 20
- PNX20
- PNX 20
- Epigenetic Reader Domain
- PGC-1α
- Toll-like Receptor (TLR)
- MyD88
- NF-κB
- Sirtuin
- NOD-like Receptor (NLR)
- ASCT
- Caspase
- Interleukin Related
- NADPH Oxidase
- Reactive Oxygen Species (ROS)
- STAT
- PPARγ coactivator-1α
- Nuclear factor-κB
- Nuclear factor-kappaB
- Alanine Serine Cysteine Transporters
- IL
- NOX
- GPR173
- NLRP3
- SIRT1
- TLR-4
- atherosclerosis
- mitochondrial biogenesis
- neuroinflammation
- oxidative stress
- Inhibitor
- inhibitor
- inhibit