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Merck

D8696

Sigma-Aldrich

DMH4

>99.0% (HPLC)

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About This Item

经验公式(希尔记法):
C24H24 N4O2
分子量:
400.47
MDL號碼:
分類程式碼代碼:
12352200
PubChem物質ID:
NACRES:
NA.77

化驗

>99.0% (HPLC)

形狀

powder

儲存條件

desiccated

顏色

off-white to brown

溶解度

DMSO: 20 mg/mL

起源

Merck & Co., Inc., Kenilworth, NJ, U.S.

儲存溫度

2-8°C

SMILES 字串

C1CN(CCO1)CCOc2ccc(cc2)-c3cnc4c(cnn4c3)-c5ccccc5

InChI

1S/C24H24N4O2/c1-2-4-20(5-3-1)23-17-26-28-18-21(16-25-24(23)28)19-6-8-22(9-7-19)30-15-12-27-10-13-29-14-11-27/h1-9,16-18H,10-15H2

InChI 密鑰

SKZQZGSPYYHTQG-UHFFFAOYSA-N

生化/生理作用

DMH4 is a potent VEGF inhibitor and an angiogenesis inhbitor. It is a selective VEGF inhibitor with an IC50 of 161 nM for VEGFR inhibition compared to 8000 nM for AMPK. Unlike the structurally similar DMH1, which is a selective BMP inhibitor, DMH4 shows little affinitiy for BMP with an IC50 of 3500 nM for BMPR-I.

特點和優勢

This compound is a featured product for Kinase Phosphatase Biology research. Click here to discover more featured Kinase Phosphatase Biology products. Learn more about bioactive small molecules for other areas of research at sigma.com/discover-bsm.
This compound was developed by Merck & Co., Inc., Kenilworth, NJ, U.S.. To browse the list of other pharma-developed compounds and Approved Drugs/Drug Candidates, click here.

象形圖

Exclamation mark

訊號詞

Warning

危險聲明

危險分類

Acute Tox. 4 Oral

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


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Eric M Erkenbrack et al.
Journal of experimental zoology. Part B, Molecular and developmental evolution, 328(5), 423-432 (2017-05-26)
Comparative studies of early development in echinoderms are revealing the tempo and mode of alterations to developmental gene regulatory networks and to the cell types they specify. In euechinoid sea urchins, skeletogenic mesenchyme (SM) ingresses prior to gastrulation at the
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Arteriosclerosis, thrombosis, and vascular biology, 39(7), 1402-1418 (2019-06-27)
Objective- Pathological neovascularization is crucial for progression and morbidity of serious diseases such as cancer, diabetic retinopathy, and age-related macular degeneration. While mechanisms of ongoing pathological neovascularization have been extensively studied, the initiating pathological vascular remodeling (PVR) events, which precede
Sungwoon Lee et al.
The Journal of clinical investigation, 127(2), 457-471 (2016-12-20)
Controlled angiogenesis and lymphangiogenesis are essential for tissue development, function, and repair. However, aberrant neovascularization is an essential pathogenic mechanism in many human diseases, including diseases involving tumor growth and survival. Here, we have demonstrated that mice deficient in C-type
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Biochimica et biophysica acta, 1853(5), 1154-1164 (2015-02-24)
We previously identified peptide Lv, a novel bioactive peptide that enhances the activity of L-type voltage-gated calcium channels (L-VGCCs) in cone photoreceptors. In this study, we verified that peptide Lv was able to augment L-VGCC currents in cardiomyocytes, as well

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