SP16 peptide
SP16 peptide is a LRP1 signaling-activating peptide and anti-inflammatory agent that crosses the blood-brain barrier. SP16 peptide activates the Akt/ERK pro-survival signaling pathway, downregulates TLR4, and inhibits NF-κB, inflammasome formation, ROS production, pro-apoptotic signaling, caspase activity, and inflammatory cytokine release. SP16 peptide exhibits cardioprotective, neuroprotective, and analgesic effects, attenuating myocardial injury and preserving left ventricular function while alleviating allodynia and nociceptive behavior. SP16 peptide restores HIV-impaired barrier integrity and reduces HIV replication and cytokine and chemokine secretion. SP16 peptide can be used in research related to acute myocardial infarction, acute pain, inflammatory and neuropathic pain, HIV infection, and non-alcoholic fatty liver disease.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- CAS. Nr.: 2640117-95-7
- Formel: C102H160N24O24
- Molecular Weight:2106.51
-
Speicherung:
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]
-
Biologische Aktivität
-
Chemical Information
- Protokoll
- Reinheit & Dokumentation
- Verweise
-
Help & FAQs
Alle Caspase Isoform-spezifische Produkte anzeigen
More
Biologische Aktivität
Beschreibung
In Vitro
SP16 peptide (25-100 µg/mL; 12 h) reduces MCP-1, RANTES, and IL-6 secretion in primary human astrocytes, and this effect is reversed by an anti-LRP1 blocking antibody, confirming LRP1 dependence[3].
SP16 peptide (1-150 µg/mL; 6-12 h) reduces p24 and decreases HIV-induced MCP-1 in HIV-1 SF162-infected primary human astrocytes[3].
SP16 peptide (25-250 µg/mL; 12 h) reduces MCP-1, IL-8, and p24 in HIV-1 SF162-infected primary human BMECs[3].
SP16 peptide (0-500 ng/mL) promotes neurite outgrowth and neuronal survival in primary adult rat DRG neurons[2].
SP16 peptide increases GAP-43 mRNA in primary adult rat DRG cultures[2].
SP16 peptide (2.4-240 nM; 5-30 min) activates Akt and ERK1/2 in rat PC12 cells, but GST-RAP blocks this activation[2].
SP16 peptide (48 h) activation of ERK1/2 in rat PC12 cells requires LRP1, and siLRP1 reduces LRP1 mRNA by 70%[2].
SP16 peptide (25-250 µg/mL; 24-96 h) does not reduce the viability of HMC3 microglia or primary human astrocytes and BMECs[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Cell Line:J774A.1 macrophages
-
Concentration:100 μg/mL
-
Incubation Time:4 h (LPS or Gp96); 2 h (Nigericin (HY-127019) or ATP (HY-B2176))
-
Result:Inhibited mature IL-1β levels by >50% following stimulation with LPS and Nigericin or Gp96 and ATP.
-
Cell Line:rat PC12 cells
-
Concentration:2.4, 24, 240 nM
-
Incubation Time:5, 10 and 30 min
-
Result:Activated phospho-ERK1/2 at concentrations as low as 24 nM.
Robustly activated ERK1/2 from 5-30 min.
Activated Akt and ERK1/2 in PC12 cells, and addition of GST-RAP blocked activation of both Akt and ERK1/2.
-
Cell Line:HMC3 microglia infected or not infected with HIV-1 SF162, cultured with and without BBB inserts
-
Concentration:1 and 100 µg/mL
-
Incubation Time:12 h
-
Result:MCP-1 secretion decreased by more than 50% in both non-infected and HIV-infected microglia with and without BBB inserts; the decrease was concentration-dependent.
IL-6 and IL-8 secretion decreased in supernatant from microglia without the BBB insert.
p24 was attenuated in a concentration-dependent manner in microglia without the BBB insert.
In cells with BBB inserts, IL-6, IL-8, and p24 were unaffected.
Parmacokinetics
In Vivo
SP16 peptide (2 μg/g; subcutaneous injection; single injection 1 hr before capsaicin injection) attenuates capsaicin-induced acute nociceptive behavior in male and female mice[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Animal Model:BALB/c (female)[1]
-
Dosage:doses of 4
μg, total of 12 μg -
Administration:i.p.; at -2 h, 0 h, and 0.5 h before LPS challenge; monitored for 72 h
-
Result:Mortality at 72 h decreased from 100% to 40%.
-
Animal Model:CD1 (outbred, male, 10 weeks of age)[1]
-
Dosage:10 µg; 100 µg
-
Administration:i.p.; immediately after reperfusion
-
Result:Infarct size was 7% of left ventricle, and cardiac troponin I at 24 h was 1.0 ng/mL.
Myocardial pAkt/total Akt ratio increased and Bax/Bcl2 ratio and caspase-3 activity decreased after 30 min ischemia and 180 min reperfusion.
At 7 days, left ventricular fractional shortening was greater and wall-motion abnormality was smaller; hearts showed reduced fibrotic scar, reduced cardiomyocyte apoptosis in the peri-infarct border zone, and reduced leukocyte infiltration.
The infarct-sparing effect was eliminated by LRP1 blocking antibody.
-
Animal Model:CD1 (outbred, male, 10 weeks of age)[1]
-
Dosage:3 µg; 10 µg; 100 µg; 500 µg
-
Administration:s.c.; after reperfusion; single dose
-
Result:Subcutaneous administration after reperfusion produced a similar reduction in infarct size to corresponding intraperitoneal doses.
-
Animal Model:C57BL/6J (male, 8-12 weeks old, 25 g)[2]
-
Dosage:0.02 μg/g; 0.2 μg/g; 2 μg/g
-
Administration:s.c.; single administration 1 hr before intraplantar formalin
-
Result:Early-phase licking time was 80 s at 0.02 μg/g and 60 s at 2 μg/g.
In the late phase, 0.2 μg/g and 2 μg/g reduced licking time; 2 μg/g delayed the late-phase peak start to 30 min.
-
Animal Model:C57BL/6J (male and female, 8-12 weeks old, 25 g)[2]
-
Dosage:2 μg/g
-
Administration:s.c.; single administration 1 hr before capsaicin
-
Result:Blocked capsaicin-induced acute pain-related behavior in male mice and produced similar effects in female mice.
-
Animal Model:C57BL/6J (male, 8-12 weeks old, 25 g)[2]
-
Dosage:2 μg/g (100 μL)
-
Administration:s.c.; daily; 1 hr before PNL and then for 2 weeks
-
Result:Prevented development of tactile allodynia; the anti-allodynic effect was most pronounced on days 2 and 4 and sustained through day 9.
In injured sciatic nerve, reduced CD11b levels by 10-fold and completely blocked injury-induced TLR4 upregulation.
In injured L4 DRGs, mice had approximately 5-fold less CD11b immunoreactivity and a 6-fold decrease in GFAP levels.
-
Animal Model:C57BL/6J (male, 4-6 months old)[3]
-
Dosage:10 µg/kg
-
Administration:intranasal; every other day; until day 5 after cART initiation
-
Result:In EcoHIV-infected mouse brains, MCP-1 was reduced by 48% versus cART alone and RANTES was reduced by 35% versus cART alone.
p24 gag was further reduced by 19% relative to cART alone.
NF-κB protein was reduced by about 86% versus cART alone and Akt protein was increased by about 18% versus cART alone.
LRP-1 expression increased.
-
Animal Model:DIAMOND (male; 2 months old at diet initiation)[4]
-
Dosage:60 µg/mouse
-
Administration:i.p.; three times per week; 12 weeks
-
Result:Serum inflammatory cytokines/chemokines were modulated after initiation at 16 weeks of WD.
-
Animal Model:DIAMOND (male; 2 months old at diet initiation)[4]
-
Dosage:100 µg/mouse; 120 µg/mouse
-
Administration:i.p.; 120 μg/mouse; three times per week; 5 weeks; i.p.; 100 μg/mouse; three times per week; 7 weeks; s.c.; 120 μg/mouse; twice per week; until sacrifice
-
Result:Prevented NAFLD-induced CD4+ T-cell depletion in the liver and spleen, confirmed by IHC.
Shifted hepatic and splenic CD4+/CD8+ T cells toward a predominant CD4+>CD8+ pattern.
Did not significantly affect the hepatic or splenic M1>M2 macrophage, NKT>NK, or predominant Te CD4+/CD8+ patterns.
Increased splenic MDSC percentage but not hepatic MDSC.
Hepatic CD4+ T-cell subsets shifted from Th1>Th2=Th17=Treg to Th1>Th2=Treg>Th17; splenic CD4+ T-cell subsets shifted from Th1=Treg>Th2=Th17 to Th1=Th2=Treg>Th17.
No serum cytokines/chemokines were significantly modulated after 48 weeks of WD.
5/6 animals were tumor-bearing and 1/6 were tumor-free.
Did not affect body weight or liver steatosis.
- Research Protocol for Infectious Diseases
- Detection of Apoptosis
- ROS/oxidative-stress fluorescent staining
- Apoptosis Solutions
- Transepithelial/transendothelial electrical resistance assay
- Research Protocol for Cardiovascular Diseases
- Research Protocol for Inflammation-related Diseases
- Research Protocol for Metabolic Diseases
- Pyroptosis Solutions
Chemical Information
-
CAS. Nr. 2640117-95-7
-
Molecular Weight 2106.51
-
Formel C102H160N24O24
-
SMILES
O=C(N[C@@H](C(C)C)C(N[C@@H](CCCCN)C(N[C@@H](CC1=CC=CC=C1)C(N[C@@H](CC(N)=O)C(N[C@@H](CCCCN)C(N2[C@@H](CCC2)C(N[C@@H](CC3=CC=CC=C3)C(N[C@@H](C(C)C)C(N[C@@H](CC4=CC=CC=C4)C(N[C@@H](CC(C)C)C(N[C@@H](CCCC)C(N[C@@H]([C@@H](C)CC)C(N[C@@H](CCC(O)=O)C(N[C@@H](CCC(N)=O)C(N[C@@H](CC(N)=O)C(N[C@@H]([C@H](O)C)C(N[C@@H](CCCCN)C(N)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)C
-
Sequence
Ac-Val-Lys-Phe-Asn-Lys-Pro-Phe-Val-Phe-Leu-Nle-Ile-Glu-Gln-Asn-Thr-Lys-NH2
-
Sequence Shortening
Ac-VKFNKPFVFL-Nle-IEQNTK-NH2
-
Versand
Room temperature in continental US; may vary elsewhere.
-
Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Reinheit & Dokumentation
Verweise
[1]. Toldo S, et al. Low-Density Lipoprotein Receptor-Related Protein-1 Is a Therapeutic Target in Acute Myocardial Infarction. JACC Basic Transl Sci. 2017 Oct 30;2(5):561-574. [Content Brief]
[2]. Wang Z, et al. α1-Antitrypsin derived SP16 peptide demonstrates efficacy in rodent models of acute and neuropathic pain. FASEB journal : official publication of the Federation of American Societies for Experimental Biology. 2022 Jan;36(1):e22093. [Content Brief]
[3]. Soler Y, et al. SERPIN-Derived Small Peptide (SP16) as a Potential Therapeutic Agent against HIV-Induced Inflammatory Molecules and Viral Replication in Cells of the Central Nervous System. Cells. 2023 Feb 15;12(4):632. [Content Brief]
[4]. Isbell M, et al. Restoration of CD4 T Cells during NAFLD without Modulation of the Hepatic Immunological Pattern Is Not Sufficient to Prevent HCC. Cancers. 2022 Nov 09;14(22):5502. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
SP16 peptide Related Classifications
HY-P12399 Related Classifications
Powered by Bioz
Keywords
- SP16 peptide
- 2640117-95-7
- LDLR
- Akt
- ERK
- Toll-like Receptor (TLR)
- NF-κB
- Caspase
- NOD-like Receptor (NLR)
- Interleukin Related
- HIV
- Low-density lipoprotein receptor
- PKB
- Protein kinase B
- Extracellular signal regulated kinases
- Nuclear factor-κB
- Nuclear factor-kappaB
- IL
- Human immunodeficiency virus
- LRP1
- NLRP3 inflammasome
- PI3K
- TLR4
- apoptosis
- blood-brain barrier
- reactive oxygen species
- Inhibitor
- inhibitor
- inhibit