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Merck
CN

F9803

Sigma-Aldrich

FTI-277 三氟乙酸盐

≥95% (HPLC), film

别名:

N-[4-[2(R)-氨基-3-巯基丙基]氨基-2-苯基苯甲酰基]蛋氨酸甲酯 三氟乙酸盐

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About This Item

经验公式(希尔记法):
C22H29N3O3S2 · xC2HF3O2
分子量:
447.61 (free base basis)
MDL编号:
UNSPSC代码:
51111800
PubChem化学物质编号:
NACRES:
NA.77

质量水平

方案

≥95% (HPLC)

表单

film

储存条件

desiccated

溶解性

H2O: ≥2 mg/mL

运输

dry ice

储存温度

−70°C

SMILES字符串

OC(=O)C(F)(F)F.COC(=O)[C@H](CCSC)NC(=O)c1ccc(NC[C@@H](N)CS)cc1-c2ccccc2

InChI

1S/C22H29N3O3S2.C2HF3O2/c1-28-22(27)20(10-11-30-2)25-21(26)18-9-8-17(24-13-16(23)14-29)12-19(18)15-6-4-3-5-7-15;3-2(4,5)1(6)7/h3-9,12,16,20,24,29H,10-11,13-14,23H2,1-2H3,(H,25,26);(H,6,7)/t16-,20+;/m1./s1

InChI key

GJEFFRDWFVSCOJ-PXPMWPIZSA-N

应用

法呢基转移酶抑制剂277(FTI-277)已被用于
  • 在乳腺癌细胞系中抑制蛋白法呢基化。
  • 骨髓分离的成人多系诱导细胞(MIAMI)中。
  • 在与带有SV40基因细胞(COS-7)的起源中抑制CV-1中的法呢基转移酶。

生化/生理作用

可拮抗H和K-Ras致癌信号的强效(pM/nM)Ras CAAX拟肽。 法呢基转移酶(Ftase)抑制剂IC50 = 50 nM。
法呢基转移酶抑制剂277(FTI-277)可介导多发性骨髓瘤的细胞凋亡,并被认为是一种潜在的治疗剂。

包装

极易吸湿材料,与脱氧的MeOH一起包装在干燥的房间中,并抽走溶剂。与干燥剂一起储存。

象形图

Exclamation mark

警示用语:

Warning

危险声明

危险分类

Eye Irrit. 2 - Skin Irrit. 2 - STOT SE 3

靶器官

Respiratory system

储存分类代码

11 - Combustible Solids

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable

个人防护装备

dust mask type N95 (US), Eyeshields, Gloves


历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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访问文档库

Endothelial protective genes induced by statin is mimicked by FTI-277 and GGTI-298 drug combination-mediated ERK5 activation
Chu UB, et al.
Biochimica et Biophysica Acta, 1850(7), 1415-1425 (2015)
The farnesyl transferase inhibitor, FTI-277, inhibits growth and induces apoptosis in drug-resistant myeloma tumor cells
Bolick SCE, et al.
Leukemia, 17(2), 451-457 (2003)
Progerin expression disrupts critical adult stem cell functions involved in tissue repair
Pacheco LM, et al.
Aging (Albany. NY.), 6(12), 1049-1063 (2014)
Daisuke Tsuji et al.
Biochemical and biophysical research communications, 556, 93-98 (2021-04-13)
Sepsis remains a leading cause of mortality in critically ill patients and is characterized by multi-organ dysfunction. Mitochondrial damage has been proposed to be involved in the pathophysiology of sepsis. In addition to metabolic impairments resulting from mitochondrial dysfunction, mitochondrial
Bingchen Han et al.
Molecular therapy : the journal of the American Society of Gene Therapy, 30(2), 672-687 (2021-07-19)
Triple-negative breast cancer (TNBC) has a high propensity for organ-specific metastasis. However, the underlying mechanisms are not well understood. Here we show that the primary TNBC tumor-derived C-X-C motif chemokines 1/2/8 (CXCL1/2/8) stimulate lung-resident fibroblasts to produce the C-C motif

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