2. Apoptosis Immunology/Inflammation
  3. Pyroptosis
  4. SK56

SK56 是一种 GSDMD-NT 孔道抑制剂。SK56 可抑制巨噬细胞和人外周血白细胞的焦亡 (Pyroptosis) 以及焦亡相关细胞因子释放。SK56 在类器官-巨噬细胞共培养模型中防止人肺泡类器官出现广泛细胞死亡。SK56 可预防 LPS (HY-D1056) 或盲肠结扎穿孔术诱导的小鼠感染性休克死亡。SK56 可用于脓毒症的相关研究。

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Custom Peptide Synthesis

SK56

SK56 Chemical Structure

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SK56 相关抗体

Top Publications Citing Use of Products

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

SK56 is a GSDMD-NT pore inhibitor. SK56 inhibits pyroptosis (Pyroptosis) and the release of pyroptosis-related cytokines in macrophages and human peripheral blood leukocytes. SK56 prevents extensive cell death in human alveolar organoids in an organoid-macrophage co-culture model. SK56 prevents death from infectious shock induced by LPS (HY-D1056) or cecal ligation and puncture in mice. SK56 can be used in studies related to sepsis[1].

体外研究
(In Vitro)

SK56 (15 μM, 2 h) 在 LPS + nigericin 诱导的 THP-1 细胞中可强烈抑制 IL-1β 和 IL-18 的释放，抑制焦亡 (IC50 = 1.38 μM) 和焦亡细胞膜片段的释放[1]。
SK56 (0.5-15 μM, 0-300 min) 在 LPS + nigericin 诱导的 BMDMs 中以浓度依赖的方式提升细胞内 ATP 水平，并通过募集 ESCRT 抑制焦亡 (IC50 = 1.12 μM)[1]。
SK56 (15 μM; 0-70 min) 在 LPS + nigericin 诱导的 THP-1 细胞中通过 GSDMD-NT 孔进入细胞，随后与线粒体结合、抑制ROS 积累，延迟乳酸脱氢酶的释放，并缓解线粒体损伤[1]。
SK56 对 GSDMC-NT-GFP (Kd 约为 0.22 µM) 和 GSDMD-NT-GFP (Kd 约为 0.25 µM) 具有强亲和力，在 PDA 纳米颗粒水凝胶中阻断由 GSDMD-NT 形成的孔道[1]。
SK56 (20 μM, 2 h) 在 LPS + nigericin 诱导的 GSDMD-casp–BFP 转染的 BMDMs 中抑制焦亡细胞膜片段上 GSDMD-NT 孔道被 BMDCs 吞噬[1]。
SK56 (20 μM, 12 h) 减少活化的 BMDCs 中 IL-1β 的分泌[1]。
SK56 (15 μM, 0.5-16 h) 在 LPS + nigericin 诱导的人肺泡类器官和 THP-1 细胞的共培养系统中抑制广泛的细胞焦亡并保护肺组织[1]。

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

SK56 相关抗体:

Western Blot Analysis[1]

Cell Line: THP-1 cells
Concentration: 15, 45 μM
Incubation Time: 2 h
Result: Exhibited the strongest inhibition of IL-1β.
Inhibited the release of GSDMD-NT in the supernatant by 80% compared to PBS at 45 μM.

Immunofluorescence[1]

Cell Line: LPS + nigericin-induced THP-1 cells
Concentration: 15 μM
Incubation Time: 0， 20，30, 40,
50, 60, 80 min
Result: Delayed pyroptosis by about 40 min.
Inhibited SYTOX green influx.
Entered cells through GSDMD-NT pores and subsequently bind to mitochondria, inhibited the decline in MitoTracker red fluorescence by 40%.

Immunofluorescence[1]

Cell Line: LPS + nigericin-induced GSDMD-casp–BFP transfectedBMDMs
Concentration: 20 μM
Incubation Time: 2 h
Result: Inhibited phagocytosis of BMDCs by GSDMD-NT pores on pyroptosis cell membrane fragments.

Immunofluorescence[1]

Cell Line: LPS + nigericin-induced alveolar organoids and THP-1 cells coculture system
Concentration: 15 μM
Incubation Time: 0.5, 4, 8, 12, 16 h
Result: Reduced the fluorescence delay of calcein-acetoxymethyl ester+ in organoids and THP-1 cells by 50%, and increased the fluorescence delay of PI+ in organoids and THP-1 cells by approximately 8 h.
Reduced the percentage of GSDMD-NT⁺ cells.

ELISA Assay[1]

Cell Line: LPS + nigericin-induced alveolar organoids and THP-1 cells coculture system
Concentration: 15 μM
Incubation Time: 12 h
Result: Inhibited IL-1β release by approximately 60% compared to PBS at 12 h.
药代动力学
(Parmacokinetics)
Species Dose Route Indicator value
Mice[1] 1 mg/kg i.v. T1/2 2.66 h
Mice[1] 1 mg/kg i.v. Tmax 0.08 h
Mice[1] 1 mg/kg i.v. Cmax 11.23 μg/mL
Mice[1] 1 mg/kg i.v. AUC0-last 22.827 μg·h/mL
Mice[1] 1 mg/kg i.v. Vss 1.308 μg/mL
Mice[1] 1 mg/kg i.v. MRT0-inf 3.351 h
体内研究
(In Vivo)

SK56 (1-4 mg/kg；静脉注射；LPS 处理后 4、5、16 h) 可在 LPS 诱导的脓毒症小鼠模型中提升生存率、减轻器官损伤与全身性炎症，并调控免疫细胞亚群[1]。
SK56 (1 mg/kg; i.v.; 16 h post-CLP) 在盲肠结扎穿孔术 (CLP) 诱导的脓毒症小鼠模型中可通过提高小鼠存活率、减轻器官损伤及降低全身细胞因子水平，发挥保护作用[1]。

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

Animal Model: C57BL/6J mice, WT/Gsdmd−/− (8-10 weeks old, 50:50 female:male ratio, LPS-induced sepsis)[1]
Dosage: 1 mg/kg (post-LPS 15 mg/kg); 2 mg/kg (post-LPS 25 mg/kg); 4 mg/kg (post-LPS 50 mg/kg)
Administration: i.v.; 16 h post-LPS; 5 h post-LPS 25 mg/kg; 4 h post-LPS 50 mg/kg
Result: Reduced mortality, alleviated damage to the kidneys, liver, intestines, spleen, and lungs, decreased the expression levels of AST, BUN, ALT, and CK, and reduced the levels of CSF2, IFNγ, IL-1β, IL-2, IL-10, and TNF in peripheral blood.
Reduced the increase of splenic mononuclear cells, inhibited the increase of lung T cells, and restored the number of total immune cells and B cells in peripheral blood.
Animal Model: C57BL/6J mice, WT/Gsdmd−/− (8-10 weeks old, 50:50 female:male ratio, CLP-induced sepsis)[1]
Dosage: 1 mg/kg
Administration: i.v.; 16 h post-CLP
Result: Reduced mortality, alleviated organ damage, decreased the expression levels of blood cytokines CSF2, IL-1β, IL-4, IL-10, and TNF, and reduced the levels of organ damage markers.
分子量

6532.50

Formula

C289H479N79O88S2
Sequence

Ser-Leu-Glu-Glu-Phe-Ala-Lys-Arg-Val-Val-Glu-Glu-Leu-Val-Lys-Glu-Phe-Asn-Leu-Asp-Lys-Arg-Gln-Glu-Ser-Tyr-Leu-Glu-Met-Ser-Ala-Leu-Ile-Gln-Ala-Gln-Met-Gly-Ile-Ser-Glu-Arg-Ile-Ile-Glu-Ile-Val-Leu-Arg-His-Ala-Ala-Gln-Thr-Leu-Lys
Sequence Shortening

SLEEFAKRVVEELVKEFNLDKRQESYLEMSALIQAQMGISERIIEIVLRHAAQTLK
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

SK56 相关分类

  • 摩尔计算器

  • 稀释计算器

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

SK56SK 56SK-56PyroptosisGSDMD-NT pore inhibitormacrophagesperipheral blood leukocytessepsis
Inhibitorinhibitorinhibit

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