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Merck
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文件

SML0429

Sigma-Aldrich

Ac-YVAD-cmk

≥95% (HPLC)

别名:

Ac-Tyr-Val-Ala-Asp-氯甲基酮肽, N-乙酰基-L-酪氨酰-L-缬氨酰-N-[(1S)-1-(羧甲基）-3-氯-2-氧基丙基]-L-丙氨酰胺, N-乙酰基-酪氨酰-缬氨酰-丙氨酰-天冬氨酰 氯甲基酮肽

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About This Item

经验公式（希尔记法）:
C24H33ClN4O8
CAS号:
178603-78-6
分子量:
540.99
MDL號碼:
MFCD00237124
分類程式碼代碼:
12352200
PubChem物質ID:
329825424
NACRES:
NA.77

化驗

≥95% (HPLC)

形狀

powder

顏色

white to off-white

運輸包裝

wet ice

儲存溫度

−20°C

SMILES 字串

CC(C)[C@H](NC(=O)[C@H](Cc1ccc(O)cc1)NC(C)=O)C(=O)N[C@@H](C)C(=O)N[C@@H](CC(O)=O)C(=O)CCl

InChI

1S/C24H33ClN4O8/c1-12(2)21(24(37)26-13(3)22(35)28-17(10-20(33)34)19(32)11-25)29-23(36)18(27-14(4)30)9-15-5-7-16(31)8-6-15/h5-8,12-13,17-18,21,31H,9-11H2,1-4H3,(H,26,37)(H,27,30)(H,28,35)(H,29,36)(H,33,34)/t13-,17-,18-,21-/m0/s1

InChI 密鑰

UOUBHJRCKHLGFB-DGJUNBOTSA-N

Amino Acid Sequence

Ac-Tyr-Val-Ala-Asp-Chloromethylketone

應用

Ac-YVAD-cmk用作：
  • 用作炎症体抑制剂，在刺激前加入THP-1细胞或PBMC（外周血单个核细胞）
  • 用作caspase-1抑制剂，注射进C57BL / 6小鼠体内
  • 用作caspase-1抑制剂，在造血干细胞移植（HSCT）前和移植期间给药小鼠，评估其对骨髓炎性损伤的影响
  • 消除富含组氨酸蛋白II (HRPII)对内皮细胞跨膜电阻（TEER）的影响
  • 用作caspase-1抑制剂，治疗MCF-7肿瘤异种移植小鼠，验证体内条件下，炎症体激活在肿瘤生长中的作用

生化／生理作用

Ac-YVAD-cmk是半胱氨酸蛋白酶-1（白细胞介素-1β 转化酶，ICE）的不可以抑制剂，具有抗半胱氨酸蛋白酶-4活性。Ac-YVAD-cmk具有抗凋亡，抗炎症和神经保护效果，它是通过阻止前半胱氨酸蛋白酶-1活化炎性细胞因子，白细胞介素-1β来起作用。

特點和優勢

该化合物是细胞凋亡研究的特色产品。点击此处 ，查看更多细胞凋亡精选产品。想要了解有关生物活性小分子在其他研究领域应用的更多信息，请访问sigma.com/discover-bsm。

儲存類別代碼

11 - Combustible Solids

水污染物質分類（WGK）

WGK 3

閃點（°F）

Not applicable

閃點（°C）

Not applicable

分析证书(COA)

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Sakshi Mehta et al.
International immunopharmacology, 88, 107013-107013 (2020-11-14)
Smoking induces excessive inflammation which is associated with all the stages of atherosclerosis. Earlier, we reported Nod-like receptor protein 3 (NLRP3) inflammasome activation as a pro-atherosclerotic property of cigarette smoking. In the present study, we aimed to explore the underlying
Plasmodium falciparum histidine-rich protein II compromises brain endothelial barriers and may promote cerebral malaria pathogenesis
Pal P, et al.
mBio, 7(3), e00617-e00616 (2016)
Growth of breast cancer cells by leptin is mediated via activation of the inflammasome: Critical roles of estrogen receptor signaling and reactive oxygen species production
Raut P K, et al.
Biochemical Pharmacology, 161, 73-88 (2019)
Sakshi Mehta et al.
Cellular signalling, 72, 109645-109645 (2020-04-20)
Smoking is known to affect all the phases of atherosclerosis, thus is considered as an independent and major risk factor. The underlying mechanism responsible for the atherogenic effects of smoking is still uncertain and a major concern. Recent evidence implicates
TLR and NLRP3 inflammasome-dependent innate immune responses to tumor-derived autophagosomes (DRibbles)
Xing Y, et al.
Cell Death & Disease, 7(8), e2322-e2322 (2016)
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