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D8696

Sigma-Aldrich

DMH4

>99.0% (HPLC)

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About This Item

Empirical Formula (Hill Notation):
C24H24 N4O2
CAS Number:
515880-75-8
Molecular Weight:
400.47
MDL number:
MFCD18452839
UNSPSC Code:
12352200
PubChem Substance ID:
329798880
NACRES:
NA.77

Assay

>99.0% (HPLC)

form

powder

storage condition

desiccated

color

off-white to brown

solubility

DMSO: 20 mg/mL

originator

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

storage temp.

2-8°C

SMILES string

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 key

SKZQZGSPYYHTQG-UHFFFAOYSA-N

Biochem/physiol Actions

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.
DMH4 is a potent selective VEGF inhibitor; angiogenesis inhibitor.

Features and Benefits

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.

Pictograms

Exclamation mark
GHS07

Signal Word

Warning

Hazard Statements

H302

Hazard Classifications

Acute Tox. 4 Oral

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

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Certificates of Analysis (COA)

Lot/Batch Number
100M4617V
100M4617

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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
Zaheer Ali et al.
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
Liheng Shi et al.
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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