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AB144222

Chetomin, HIF signaling inhibitor

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(1 Publication)

MW 710.9 Da, Purity >98%. Potent HIF signaling inhibitor. Reduces CA9 and VEGF expression in hypoxic cells (IC50 = 10 nM, secreted VEGF, Hep38 cells). Shows antibacterial and antifungal effects. Shows antitumor effects in vivo. .

View Alternative Names

H3-K9-HMTase 1, Histone H3-K9 methyltransferase1, Histone lysine N methyltransferase, H3 lysine 9 specific 1, Histone-lysine N-methyltransferase SUV39H1, KMT1 A, Lysine N-methyltransferase 1A, MG44, Position-effect variegation 3-9 homolog, SUV39 H1, SUV39H, SUV91_HUMAN, Su(var)3-9 homolog 1, Suppressor of variegation 3 9 homolog 1 (Drosophila), Suppressor of variegation 3-9 homolog 1, mIS6

1 Images
Chemical Structure - Chetomin, HIF signaling inhibitor (AB144222)
  • Chemical Structure

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Chemical Structure - Chetomin, HIF signaling inhibitor (AB144222)

2D chemical structure image of ab144222, Chetomin, HIF signaling inhibitor

Key facts

CAS number

1403-36-7

Purity

>98%

Form

Solid

form

Source

Chaetomium sp.

Molecular weight

710.9 Da

Molecular formula

C<sub>3</sub><sub>1</sub>H<sub>3</sub><sub>0</sub>N<sub>6</sub>O<sub>6</sub>S<sub>4</sub>

PubChem

10417379

Nature

Native

Solubility

Soluble in DMSO

Biochemical name

Chetomin

Biological description

Potent HIF signaling inhibitor. Reduces CA9 and VEGF expression in hypoxic cells (IC50 = 10 nM, secreted VEGF, Hep38 cells). Shows antibacterial and antifungal effects. Shows antitumor effects in vivo.

Canonical smiles

CN1C(=O)C2(N(C(=O)C1(SS2)CC3=CN(C4=CC=CC=C43)C56CC78C(=O)N(C(C(=O)N7C5NC9=CC=CC=C69)(SS8)CO)C)C)CO

Isomeric smiles

CN1C(=O)[C@]2(N(C(=O)[C@@]1(SS2)CC3=CN(C4=CC=CC=C43)[C@]56C[C@]78C(=O)N([C@](C(=O)N7[C@H]5NC9=CC=CC=C69)(SS8)CO)C)C)CO

InChi

InChI=1S/C31H30N6O6S4/c1-33-25(42)30(15-38)34(2)23(40)28(33,44-46-30)12-17-13-36(21-11-7-4-8-18(17)21)27-14-29-24(41)35(3)31(16-39,47-45-29)26(43)37(29)22(27)32-20-10-6-5-9-19(20)27/h4-11,13,22,32,38-39H,12,14-16H2,1-3H3/t22-,27+,28+,29+,30+,31+/m1/s1

InChiKey

ZRZWBWPDBOVIGQ-YWZWRZHGSA-N

IUPAC Name

(1S,3S,11R,14S)-14-(hydroxymethyl)-3-[3-[[(1S,4S)-4-(hydroxymethyl)-5,7-dimethyl-6,8-dioxo-2,3-dithia-5,7-diazabicyclo[2.2.2]octan-1-yl]methyl]indol-1-yl]-18-methyl-15,16-dithia-10,12,18-triazapentacyclo[12.2.2.01,12.03,11.04,9]octadeca-4,6,8-triene-13,17-dione

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Properties and storage information

Shipped at conditions
Ambient - Can Ship with Ice
Appropriate short-term storage conditions
-20°C
Appropriate long-term storage conditions
-20°C
Storage information
Store under desiccating conditions|The product can be stored for up to 12 months
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Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

KMT1A also known as SUV39H1 is a well-studied histone methyltransferase responsible for trimethylating histone H3 at lysine 9 (H3K9me3) an important marker for heterochromatin formation. This enzyme plays a critical role in chromatin organization and gene regulation. KMT1A has a molecular weight of approximately 48 kDa. Researchers have observed its expression across a range of tissues including the brain heart and muscle which suggests its importance in various physiological processes.
Biological function summary

KMT1A functions as part of a Suv39H1/HP1 complex that maintains the integrity of pericentric heterochromatin essential for chromosome stability during cell division. Its influence extends over the transcriptional silencing of specific genes by modifying chromatin structure to a closed state. KMT1A also collaborates with other proteins like HP1 to silence repetitive elements and prevent genomic instability which is often important for safeguarding genomic fidelity in cells.

Pathways

Researchers identify KMT1A as a significant player in the regulation of epigenetic pathways particularly the histone methylation process. It interacts closely with other histone methyltransferases and demethylases contributing to a dynamic epigenetic landscape that controls gene expression. Additionally KMT1A is involved in the DNA damage response pathway in collaboration with proteins like ATM which coordinates repair mechanisms to maintain genetic stability and respond to cellular stress.

Researchers have linked KMT1A with cancer and neurodegenerative diseases such as Huntington’s disease. Abnormal expression or function of KMT1A can lead to disrupted heterochromatin structure and uncontrolled gene expression which contributes to tumorigenesis. Furthermore in the context of neurodegenerative conditions interactions with proteins such as HTT can exacerbate neuronal damage and cell death. Studying these associations provides insights into potential therapeutic targets for managing such diseases.
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Product protocols

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Publications (1)

Recent publications for all applications. Explore the full list and refine your search

Frontiers in cellular and infection microbiology 7:23 PubMed28229048

2017

Infection Subverts Carbohydrate Metabolic Pathways in the Tick Vector, .

Applications

Unspecified application

Species

Unspecified reactive species

Alejandro Cabezas-Cruz,Pilar Alberdi,James J Valdés,Margarita Villar,José de la Fuente
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