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WJ460 Sale

目录号 : GC38203

WJ460 是一种有效的肌成纤维蛋白 (MYOF) 抑制剂,可与 MYOF 直接相互作用,并在乳腺癌细胞的纳摩尔范围内发挥抗转移活性。

WJ460 Chemical Structure

Cas No.:1415251-36-3

规格 价格 库存 购买数量
10mM (in 1mL DMSO)
¥1,135.00
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1mg
¥350.00
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5mg
¥1,120.00
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10mg
¥1,890.00
现货
25mg
¥3,150.00
现货
50mg
¥5,390.00
现货
100mg
¥9,100.00
现货

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Sample solution is provided at 25 µL, 10mM.

产品文档

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产品描述

WJ460 is a potent myoferlin (MYOF) inhibitor, which interacts directly with MYOF and exerts anti-metastatic activity in the nanomolar range in breast cancer cells[1].

WJ460 blocks breast cancer cell invasion with IC50 values of 43.37 ± 3.42 nM in MDA-MB-231 and 36.40 ± 4.51 nM in BT549 cells. WJ460 treatment remarkably inhibits MDA-MB-231 and BT549 cell invasion through Collagen I in a dose-dependent manner[1].

WJ460 inhibits breast tumor growth, angiogenesis, and spontaneous metastasis in a spontaneous metastasis model[1].

[1]. Zhang T, et al. A small molecule targeting myoferlin exerts promising anti-tumor effects on breast cancer. Nat Commun. 2018 Sep 13;9(1):3726.

Chemical Properties

Cas No. 1415251-36-3 SDF
Canonical SMILES O=C(NCCCCC1=CC=CC=C1)C2=CC=CC(C(N3C4=CC=CC=C4OC)SCC3=O)=C2
分子式 C27H28N2O3S 分子量 460.59
溶解度 DMSO: 250 mg/mL (542.78 mM) 储存条件 Store at -20°C
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溶解性数据

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1 mg 5 mg 10 mg
1 mM 2.1711 mL 10.8556 mL 21.7113 mL
5 mM 0.4342 mL 2.1711 mL 4.3423 mL
10 mM 0.2171 mL 1.0856 mL 2.1711 mL
460.59
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Research Update

Myoferlin targeting triggers mitophagy and primes ferroptosis in pancreatic cancer cells

Redox Biol 2022 Jul;53:102324.PMID:35533575DOI:10.1016/j.redox.2022.102324.

Myoferlin, an emerging oncoprotein, has been associated with a low survival in several cancer types including pancreas ductal adenocarcinoma where it controls mitochondria structure and respiratory functions. Owing to the high susceptibility of KRAS-mutated cancer cells to iron-dependent cell death, ferroptosis, and to the high iron content in mitochondria, we investigated the relation existing between mitochondrial integrity and iron-dependent cell death. We discovered that myoferlin targeting with WJ460 pharmacological compound triggered mitophagy and ROS accumulation culminating with lipid peroxidation and apoptosis-independent cell death. WJ460 caused a reduction of the abundance of ferroptosis core regulators xc- cystine/glutamate transporter and GPX-4. Mitophagy inhibitor Mdivi1 and iron chelators inhibited the myoferlin-related ROS production and restored cell growth. Additionally, we reported a synergic effect between ferroptosis inducers, erastin and RSL3, and WJ460.

Discovery of 1,5-diaryl-1,2,4-triazole derivatives as myoferlin inhibitors and their antitumor effects in pancreatic cancer

Future Med Chem 2022 Oct;14(20):1425-1440.PMID:36165130DOI:10.4155/fmc-2022-0168.

Aim: The first inhibitor targeting myoferlin (MYOF), WJ460, bears poor metabolic stability and water solubility. Therefore, this study aimed to improve the drug-like properties of WJ460. Materials & methods: The authors synthesized an array of 1,5-diaryl-1,2,4-triazole analogs and appraised the binding activities with MYOF and their antiproliferative and antimigratory activities against pancreatic cancer cells. Results: Molecular docking and surface plasmon resonance results showed that E4 was directly bound to the MYOF-C2D domain. E4 effectively inhibited the proliferation and migration of pancreatic cancer cells in vitro. An in silico study suggested that the water solubility of E4 was improved by about 22-times than that of WJ460. Conclusion: The findings suggested that the druglike ability of E4 was significantly improved.

A small molecule targeting myoferlin exerts promising anti-tumor effects on breast cancer

Nat Commun 2018 Sep 13;9(1):3726.PMID:30213946DOI:10.1038/s41467-018-06179-0.

Breast cancer is one of the most lethal cancers in women when it reaches the metastatic stage. Here, we screen a library of small molecules for inhibitors of breast cancer cell invasion, and use structure/activity relationship studies to develop a series of small molecules with improved activity. We find WJ460 as one of the lead compounds exerting anti-metastatic activity in the nanomolar range in breast cancer cells. Proteomic and biochemical studies identify myoferlin (MYOF) as the direct target of WJ460. In parallel, loss of MYOF or pharmacological inhibition of MYOF by WJ460 reduces breast cancer extravasation into the lung parenchyma in an experimental metastasis mouse model, which reveals an essential role of MYOF in breast cancer progression. Our findings suggest that MYOF can be explored as a molecular target in breast cancer metastasis and that targeting MYOF by WJ460 may be a promising therapeutic strategy in MYOF-driven cancers.

HBZ upregulates myoferlin expression to facilitate HTLV-1 infection

PLoS Pathog 2023 Feb 24;19(2):e1011202.PMID:36827461DOI:10.1371/journal.ppat.1011202.

The complex retrovirus, human T-cell leukemia virus type 1 (HTLV-1), primarily infects CD4+ T-cells in vivo. Infectious spread within this cell population requires direct contact between virally-infected and target cells. The HTLV-1 accessory protein, HBZ, was recently shown to enhance HTLV-1 infection by activating intracellular adhesion molecule 1 (ICAM-1) expression, which promotes binding of infected cells to target cells and facilitates formation of a virological synapse. In this study we show that HBZ additionally enhances HTLV-1 infection by activating expression of myoferlin (MyoF), which functions in membrane fusion and repair and vesicle transport. Results from ChIP assays and quantitative reverse transcriptase PCR indicate that HBZ forms a complex with c-Jun or JunB at two enhancer sites within the MYOF gene and activates transcription through recruitment of the coactivator p300/CBP. In HTLV-1-infected T-cells, specific inhibition of MyoF using the drug, WJ460, or shRNA-mediated knockdown of MyoF reduced infection efficiency. This effect was associated with a decrease in cell adhesion and an intracellular reduction in the abundance of HTLV-1 envelope (Env) surface unit (SU) and transmembrane domain (TM). Lysosomal protease inhibitors partially restored SU levels in WJ460-treated cells, and SU localization to LAMP-2 sites was increased by MyoF knockdown, suggesting that MyoF restricts SU trafficking to lysosomes for degradation. Consistent with these effects, less SU was associated with cell-free virus particles. Together, these data suggest that MyoF contributes to HTLV-1 infection through modulation of Env trafficking and cell adhesion.