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213546-53-3

中文名稱(chēng) 213546-53-3
英文名稱(chēng) NFκB Inhibitor
CAS 213546-53-3
分子式 C129H230N36O29S
分子量 2781.5
MOL 文件 213546-53-3.mol
更新日期 2026/07/27 12:41:43
213546-53-3 結(jié)構(gòu)式 213546-53-3 結(jié)構(gòu)式

基本信息

中文別名
化合物 T12942
易位抑制劑多肽SN50
H-ALA-ALA-VAL-ALA-LEU-LEU-PRO-ALA-VAL-LEU-LEU-ALA-LEU-LEU-ALA-PRO-VAL-GLN-ARG-LYS-ARG-GLN-LYS-LEU-MET-PRO-OH
英文別名
SN50
NFkB Inhibitor
NF-KAPPA-B SN50
NF-κB Inhibitor, SN50
NF-KAPPAB INHIBITOR SN50
AAVALLPAVLLALLAPVQRKRQKLMP
NF-κB Inhibitor, SN50, >=97%
NUCLEAR FACTOR NF-B INHIBITOR SN50
NUCLEAR FACTOR NF-KAPPA-B INHIBITOR SN50
NF-KAPPAB SN50, CELL-PERMEABLE INHIBITORY PEPTIDE

物理化學(xué)性質(zhì)

密度1.36±0.1 g/cm3(Predicted)
儲(chǔ)存條件-20°C
形態(tài)film
顏色無(wú)色
水溶解性Water : ≥ 50 mg/mL (17.98 mM)
序列Ala-Ala-Val-Ala-Leu-Leu-Pro-Ala-Val-Leu-Leu-Ala-Leu-Leu-Ala-Pro-Val-Gln-Arg-Lys-Arg-Gln-Lys-Leu-Met-Pro
InChIKeyFAWLNURBQMTKEB-URDPEVQOSA-N

安全數(shù)據(jù)

WGK GermanyWGK 3
存儲(chǔ)類(lèi)別11 - Combustible Solids
213546-53-3價(jià)格(試劑級(jí))
報(bào)價(jià)日期產(chǎn)品編號(hào)產(chǎn)品名稱(chēng)CAS號(hào)包裝價(jià)格
2026/07/06S6671213546-53-3
SN50
213546-53-35mg3670.55元
2026/07/06S6671213546-53-3
SN50
213546-53-325mg9450.55元
2026/07/06S6671SN50213546-53-3100mg24300.5元

常見(jiàn)問(wèn)題列表

生物活性
SN50 (NF-κB SN50)是一種可滲透細(xì)胞的NF-κB抑制肽,由Kaposi成纖維細(xì)胞生長(zhǎng)因子信號(hào)肽組成。SN50抑制NF-κB的活化并減輕呼吸機(jī)誘發(fā)的肺損傷。
靶點(diǎn)
TargetValue
NF-κB
()
體外研究

Pretreatment with SN50 results in a significant reduction in amount of PI-positive cells at 12, 24, and 48 h time-point post TBI compared with vehicle-treated groups. Topical SN50 suppresses nuclear factor-κB activation in local cells and reduces the incidence of epithelial defects/ulceration in healing corneas. Myofibroblast generation, macrophage invasion, activity of matrix metalloproteinases, basement membrane destruction, and expression of cytokines are all decreased in treated corneas compared with controls. Treating the human gastric cancer cells SGC7901 with SN50 could significantly enhance the effects of LY294002 on inducing cell death after 24 h. SN50 can inhibit translocation of NF-kB and production of inflammatory cytokines that are implicated in lipopolysaccharide (LPS)-induced lung injury.

體內(nèi)研究

Treatment with SN50 accelerates the recovery of motor functional outcome from 1st to 4th day. Animals subjected to SN50 pretreatment demonstrate a significant decrease in the visuospatial learning latencies relative to the control group at 7 and 8 days post-TBI. Pretreatment with SN50 results in a significant reduction of NF-κB p65 protein levels from 6 to 48 h post-TBI and TNF-a protein levels from 12 to 48 h post-TBI.

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