Ac-FLTD-CMK

Pricing Availability   Qty
说明: Potent and selective inhibitor of caspases 1, 5 and 4
纯度: ≥95% (HPLC)
说明书
引用文献
评论
文献 (5)

生物活性 for Ac-FLTD-CMK

Ac-FLTD-CMK is a potent and selective inhibitor of caspases 1, 5 and 4 (IC50 values = 46.7 nM, 0.33 μM, 1.49 μM, respectively), and inhibits murine caspase-11 at 10 μM. Ac-FLTD-CMK inhibits cleavage of gasdermin D by caspases, suppresses pyroptosis and reduces IL-1β release in macrophages.

技术数据 for Ac-FLTD-CMK

分子量 569.05
公式 C26H37ClN4O8
序列 FLTD

(Modifications: Phe-1 = Ac-Phe, Asp-4 = Asp-CMK)

储存 Store at -20°C
纯度 ≥95% (HPLC)
CAS Number 2376255-48-8
PubChem ID 155906572
InChI Key UCWNTWGHVCSMJP-WPUDHWPRSA-N
Smiles O=C(N[C@@H](CC(C)C)C(N[C@@H]([C@H](O)C)C(N[C@@H](CC(O)=O)C(CCl)=O)=O)=O)[C@H](CC1=CC=CC=C1)NC(C)=O

上方提供的技术数据仅供参考。批次相关数据请参见分析证书。

Tocris products are intended for laboratory research use only, unless stated otherwise.

溶解性数据 for Ac-FLTD-CMK

溶解性 Soluble to 1 mg/ml in DMSO

产品说明书 for Ac-FLTD-CMK

分析证书/产品说明书
选择另一批次:

参考文献 for Ac-FLTD-CMK

参考文献是支持产品生物活性的出版物。

Yang et al (2018) Mechanism of gasdermin D recognition by inflammatory caspases and their inhibition by a gasdermin D-derived peptide inhibitor. Proc.Natl.Acad.Sci.U.S.A. 115 6792 PMID: 29891674


If you know of a relevant reference for Ac-FLTD-CMK, please let us know.

按标靶查看相关产品

按产品操作查看相关产品

查看全部 Caspase Inhibitors

关键词: Ac-FLTD-CMK, Ac-FLTD-CMK supplier, AcFLTDCMK, potent, selective, inhibitors, inhibits, caspases, inflammasome, pyroptosis, IL-b, IL-beta, caspase1, Caspases, 7242, Tocris Bioscience

篇 Ac-FLTD-CMK 的引用文献

引用文献是使用了 Tocris 产品的出版物。

目前没有 Ac-FLTD-CMK 的引用文献。 您是否知道使用了 Tocris Ac-FLTD-CMK 的优秀论文? 请告知我们.

Ac-FLTD-CMK 的评论

目前没有该产品的评论。 Be the first to review Ac-FLTD-CMK and earn rewards!

Have you used Ac-FLTD-CMK?

Submit a review and receive an Amazon gift card.

$50/€35/£30/$50CAN/¥300 Yuan/¥5000 Yen for first to review with an image

$25/€18/£15/$25CAN/¥75 Yuan/¥2500 Yen for a review with an image

$10/€7/£6/$10 CAD/¥70 Yuan/¥1110 Yen for a review without an image

Submit a Review

该领域的文献

Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!

*请注意,Tocris 仅会向正规科研企业/机构地址发送文献。


Cell Cycle and DNA Damage Research Product Guide

Cell Cycle and DNA Damage Research Product Guide

This product guide provides a review of the cell cycle and DNA damage research area and lists over 150 products, including research tools for:

  • Cell Cycle and Mitosis
  • DNA Damage Repair
  • Targeted Protein Degradation
  • Ubiquitin Proteasome Pathway
  • Chemotherapy Targets
Cell Cycle & DNA Damage Repair Poster

Cell Cycle & DNA Damage Repair Poster

In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. This poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.

Huntington's Disease Poster

Huntington's Disease Poster

Huntington's disease (HD) is a severe monogenic neurodegenerative disorder, which is characterized by the prevalent loss of GABAergic medium spiny neurons (MSN) in the striatum. This poster summarizes the effects of mutant huntingtin aggregation implicated in the pathology of HD, as well as highlighting the use of iPSCs for HD modeling.

Parkinson's Disease Poster

Parkinson's Disease Poster

Parkinson's disease (PD) causes chronic disability and is the second most common neurodegenerative condition. This poster outlines the neurobiology of the disease, as well as highlighting current therapeutic treatments for symptomatic PD, and emerging therapeutic strategies to delay PD onset and progression.

Programmed Cell Death Poster

Programmed Cell Death Poster

There are two currently recognized forms of programmed cell death: apoptosis and necroptosis. This poster summarizes the signaling pathways involved in apoptosis, necroptosis and cell survival following death receptor activation, and highlights the influence of the molecular switch, cFLIP, on cell fate.