Melanocin A
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| Category | Enzyme inhibitors |
| Catalog number | BBF-02319 |
| CAS | |
| Molecular Weight | 338.31 |
| Molecular Formula | C18H14N2O5 |
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Description
It is produced by the strain of Eupenicillium shearii F80965. It is a Melanin biosynthesis inhibitor. It inhibits the biosynthesis of melanin and tyrosinase (IC50 is 9.0 nmol/L, MIC is 0.9 μmol/L). It also has antioxidant effect.
Specification
| IUPAC Name | N-[(1Z,3Z)-3-cyano-1,4-bis(3,4-dihydroxyphenyl)buta-1,3-dien-2-yl]formamide |
| Canonical SMILES | C1=CC(=C(C=C1C=C(C#N)C(=CC2=CC(=C(C=C2)O)O)NC=O)O)O |
| InChI | InChI=1S/C18H14N2O5/c19-9-13(5-11-1-3-15(22)17(24)7-11)14(20-10-21)6-12-2-4-16(23)18(25)8-12/h1-8,10,22-25H,(H,20,21)/b13-5+,14-6- |
| InChI Key | VDPHYDSLIYDKAP-LSMSNJBFSA-N |
Properties
| Appearance | Yellow Powder |
| Melting Point | 212°C |
| Solubility | Soluble in Methanol |
Reference Reading
1. Antiproliferative and Antimigration Activities of Fluoro-Neplanocin A via Inhibition of Histone H3 Methylation in Triple-Negative Breast Cancer
Woong Sub Byun, Won Kyung Kim, Ji-Seong Yoon, Dnyandev B Jarhad, Lak Shin Jeong, Sang Kook Lee Biomolecules. 2020 Mar 31;10(4):530. doi: 10.3390/biom10040530.
Triple-negative breast cancer (TNBC) is among the most aggressive and potentially metastatic malignancies. Most affected patients have poor clinical outcomes due to the lack of specific molecular targets on tumor cells. The upregulated expression of disruptor of telomeric silencing 1-like (DOT1L), a histone methyltransferase specific for the histone H3 lysine 79 residue (H3K79), is strongly correlated with TNBC cell aggressiveness. Therefore, DOT1L is considered a potential molecular target in TNBC. Fluoro-neplanocin A (F-NepA), an inhibitor of S-adenosylhomocysteine hydrolase, exhibited potent antiproliferative activity against various types of cancer cells, including breast cancers. However, the molecular mechanism underlying the anticancer activity of F-NepA in TNBC cells remains to be elucidated. We determined that F-NepA exhibited a higher growth-inhibitory activity against TNBC cells relative to non-TNBC breast cancer and normal breast epithelial cells. Moreover, F-NepA effectively downregulated the level of H3K79me2 in MDA-MB-231 TNBC cells by inhibiting DOT1L activity. F-NepA also significantly inhibited TNBC cell migration and invasion. These activities of F-NepA might be associated with the upregulation of E-cadherin and downregulation of N-cadherin and Vimentin in TNBC cells. Taken together, these data highlight F-NepA as a strong potential candidate for the targeted treatment of high-DOT1L-expressing TNBC.
2. Novel Neplanocin A Derivatives as Selective Inhibitors of Hepatitis B Virus with a Unique Mechanism of Action
Masaaki Toyama, Koichi Watashi, Masanori Ikeda, Atsuya Yamashita, Mika Okamoto, Kohji Moriishi, Masamichi Muramatsu, Takaji Wakita, Ashoke Sharon, Masanori Baba Antimicrob Agents Chemother. 2022 Jun 21;66(6):e0207321. doi: 10.1128/aac.02073-21. Epub 2022 May 23.
Novel neplanocin A derivatives have been identified as potent and selective inhibitors of hepatitis B virus (HBV) replication in vitro. These include (1S,2R,5R)-5-(5-bromo-4-methyl-7H-pyrrolo[2,3-d]-pyrimidin-7-yl)-3-(hydroxymethyl)cyclopent-3-ene-1,2-diol (AR-II-04-26) and (1S,2R,5R)-5-(4-amino-3-iodo-1H-pyrazolo[3,4-d]pyrimidin-1-yl)-3-(hydroxylmethyl)cyclopent-3-ene-1,2-diol (MK-III-02-03). The 50% effective concentrations of AR-II-04-26 and MK-III-02-03 were 0.77 ± 0.23 and 0.83 ± 0.36 μM in HepG2.2.15.7 cells, respectively. These compounds reduced intracellular HBV RNA levels in HepG2.2.15.7 cells and infected primary human hepatocytes. Accordingly, they could reduce HBs and HBe antigen production in the culture supernatants, which was not observed with clinically approved anti-HBV nucleosides and nucleotides (reverse transcriptase inhibitors). The neplanocin A derivatives also inhibited HBV RNA derived from cccDNA. In addition, unlike neplanocin A itself, the compounds did not inhibit S-adenosyl-l-homocysteine hydrolase activity. Thus, it appears that the mechanism of action of AR-II-04-26 and MK-III-02-03 differs from that of the clinically approved anti-HBV agents. Although their exact mechanism (target molecule) remains to be elucidated, the novel neplanocin A derivatives are considered promising candidate drugs for inhibition of HBV replication.
3. 3-Deazaneplanocin A and neplanocin A analogues and their effects on apoptotic cell death
Eric K W Tam, Tuan Minh Nguyen, Cheryl Z H Lim, Puay Leng Lee, Zhimei Li, Xia Jiang, Sridhar Santhanakrishnan, Tiong Wei Tan, Yi Ling Goh, Sze Yue Wong, Haiyan Yang, Esther H Q Ong, Jeffrey Hill, Qiang Yu, Christina L L Chai ChemMedChem. 2015 Jan;10(1):173-82. doi: 10.1002/cmdc.201402315. Epub 2014 Oct 15.
3-Deazaneplanocin A (DzNep) is a potential epigenetic drug for the treatment of various cancers. DzNep has been reported to deplete histone methylations, including oncogenic EZH2 complex, giving rise to epigenetic modifications that reactivate many silenced tumor suppressors in cancer cells. Despite its promise as an anticancer drug, little is known about the structure-activity relationships of DzNep in the context of epigenetic modifications and apoptosis induction. In this study, a number of analogues of DzNep were examined for DzNep-like ability to induce synergistic apoptosis in cancer cells in combination with trichostatin A, a known histone deacetylase (HDAC) inhibitor. The structure-activity relationship data thus obtained provide valuable information on the structural requirements for biological activity. The studies identified three compounds that show similar activities to DzNep. Two of these compounds show good pharmacokinetics and safety profiles. Attempts to correlate the observed synergistic apoptotic activities with measured S-adenosylhomocysteine hydrolase (SAHH) inhibitory activities suggest that the apoptotic activity of DzNep might not be directly due to its inhibition of SAHH.
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Bio Calculators
* Our calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
It is commonly abbreviated as: C1V1 = C2V2
* Total Molecular Weight:
g/mol
Tip: Chemical formula is case sensitive. C22H30N4O √ c22h30n40 ╳
