Chaetocin
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| Category | Antibiotics |
| Catalog number | BBF-00767 |
| CAS | 28097-03-2 |
| Molecular Weight | 696.84 |
| Molecular Formula | C30H28N6O6S4 |
| Purity | >99% by HPLC |
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Description
It is produced by the strain of Chaetomium minutum. It has the activity of anti-gram-positive bacteria and negative bacteria.
Specification
| Synonyms | Caetocin; Chetocin; 3,11a-Epidithio-11aH-pyrazino[1',2':1,5]pyrrolo[2,3-b]indole, bimol. deriv.; (+)-Chaetocin; (+)-Chaetocin A; Chaetocin A; [3S-[3α,5aβ,10bβ(3'R*,5'aS*,10'bS*,11'aR*),11aα]]-2,2',3,3',5a,5'a,6,6'-Octahydro-3,3'-bis(hydroxymethyl)-2,2'-dimethyl-[10b,10'b(11H,11'H)-Bi-3,11a-epidithio-11aH-pyrazino[1',2':1,5]pyrrolo[2,3-b]indole]-1,1',4,4'-tetrone; NSC-745363 |
| Storage | 2-8 °C |
| IUPAC Name | 14-(hydroxymethyl)-3-[14-(hydroxymethyl)-18-methyl-13,17-dioxo-15,16-dithia-10,12,18-triazapentacyclo[12.2.2.01,12.03,11.04,9]octadeca-4,6,8-trien-3-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 |
| Canonical SMILES | CN1C(=O)C23CC4(C(N2C(=O)C1(SS3)CO)NC5=CC=CC=C54)C67CC89C(=O)N(C(C(=O)N8C6NC1=CC=CC=C71)(SS9)CO)C |
| InChI | InChI=1S/C30H28N6O6S4/c1-33-21(39)27-11-25(15-7-3-5-9-17(15)31-19(25)35(27)23(41)29(33,13-37)45-43-27)26-12-28-22(40)34(2)30(14-38,46-44-28)24(42)36(28)20(26)32-18-10-6-4-8-16(18)26/h3-10,19-20,31-32,37-38H,11-14H2,1-2H3 |
| InChI Key | PZPPOCZWRGNKIR-UHFFFAOYSA-N |
| Source | Chaetomium sp. |
Properties
| Appearance | Colorless Acicular Crystal |
| Antibiotic Activity Spectrum | Gram-positive bacteria; Gram-negative bacteria |
| Melting Point | 240 °C(dec.) |
| Density | 1.87 g/cm3 |
| Solubility | Soluble in DMSO, Pyridine, Ethanol, Methanol, DMF; Poorly soluble in Water |
Reference Reading
1. Chaetocin Abrogates the Self-Renewal of Bladder Cancer Stem Cells via the Suppression of the KMT1A-GATA3-STAT3 Circuit
Changyuan Yu, Wei Zhang, Chong Li, Guoqing Wang, Haifeng Wang, Nan Zhang, Tianying Xing, Zhao Yang Front Cell Dev Biol . 2020 Jun 17;8:424. doi: 10.3389/fcell.2020.00424.
Bladder cancer stem cells (BCSCs) have the abilities of self-renewal, differentiation, and metastasis; confer drug resistance; and exhibit high tumorigenicity. We previously identified that the KMT1A-GATA3-STAT3 axis drives the self-renewal of BCSCs. However, the therapeutic effect of targeting KMT1A in BCSCs remains unknown. In this study, we confirmed that the expression of KMT1A was remarkably higher in BCSCs (3-5-fold) than those in bladder cancer non-stem cells or normal bladder epithelial cells. Among the six KMT1A inhibitors, chaetocin significantly suppressed the cell propagation (inhibition ratio: 65%-88%, IC50= 24.4-32.5 nM), induced apoptosis (2-5-fold), and caused G1 phase cell cycle arrest (68.9 vs 55.5%) of bladder cancer (BC) cells, without influencing normal bladder epithelial cells. More importantly, chaetocin abrogated the self-renewal of BCSCs (inhibition ratio: 80.1%) via the suppression of the KMT1A-GATA3-STAT3 circuit and other stemness-related pathways. Finally, intravesical instillation of chaetocin remarkably inhibited the growth of xenograft tumors (inhibition ratio: 71-82%) and prolonged the survival of tumor-bearing mice (70 vs 53 days). In sum, chaetocin abrogated the stemness maintenance and tumor growth of BCSCs via the suppression of the KMT1A-GATA3-STAT3 circuit. Chaetocin is an effective inhibitor targeting KMT1A in BCSCs and could be a promising therapeutic strategy for BC.
2. Chaetocin attenuates atherosclerosis progression and inhibits vascular smooth muscle cell phenotype switching
Ming-Yun Chen, Lian-Xi Li, Jiang-Feng Ke, Ting-Ting Li, Jun-Xi Lu, Mei-Fang Li, Zhi-Hui Zhang J Cardiovasc Transl Res . 2022 Dec;15(6):1270-1282. doi: 10.1007/s12265-022-10258-5.
We aimed to explore the effect of chaetocin on atherosclerosis and its possible mechanism. In vitro, we observed that chaetocin treatment significantly inhibited the proliferation of VSMCs in concentration- and time-dependent manner. We also found that chaetocin suppressed the migration of VSMCs. Moreover, chaetocin treatment induced a contractile phenotype in VSMCs by increasing α-SMA and SM22α expression. In addition, chaetocin treatment attenuated the accumulation of H3K9me3 on VSMCs contractile gene promoters, which promoted the expression of α-SMA and SM22α. In vivo, chaetocin treatment decreased the H3K9me3 expression, diminished atherosclerotic plaque formation, and increased plaque stability by decreasing necrotic core area and lipid accumulation and increasing collagen content and contractile VSMC phenotype. We demonstrated a new function of chaetocin in inhibiting atherosclerosis progression and increasing plaque stability partly by inhibiting pathological phenotypic switching of VSMCs. These newly identified roles of chaetocin might provide a novel therapeutic target in atherosclerosis.
3. ROS/JNK/C-Jun Pathway is Involved in Chaetocin Induced Colorectal Cancer Cells Apoptosis and Macrophage Phagocytosis Enhancement
Wende Li, Lu He, Chuangyu Wen, Siyu Chen, Weibiao Ye, Qiyuan Qin, Fang Wang, Junsheng Peng, Xiangling Yang, Huanliang Liu, Junxiong Chen, Weiqian Li, Huihui Wang Front Pharmacol . 2021 Oct 27;12:729367. doi: 10.3389/fphar.2021.729367.
There is an urgent need for novel agents for colorectal cancer (CRC) due to the increasing number of cases and drug-resistance related to current treatments. In this study, we aim to uncover the potential of chaetocin, a natural product, as a chemotherapeutic for CRC treatment. We showed that, regardless of 5-FU-resistance, chaetocin induced proliferation inhibition by causing G2/M phase arrest and caspase-dependent apoptosis in CRC cells. Mechanically, our results indicated that chaetocin could induce reactive oxygen species (ROS) accumulation and activate c-Jun N-terminal kinase (JNK)/c-Jun pathway in CRC cells. This was confirmed by which the JNK inhibitor SP600125 partially rescued CRC cells from chaetocin induced apoptosis and the ROS scavenger N-acetyl-L-cysteine (NAC) reversed both the chaetocin induced apoptosis and the JNK/c-Jun pathway activation. Additionally, this study indicated that chaetocin could down-regulate the expression of CD47 at both mRNA and protein levels, and enhance macrophages phagocytosis of CRC cells. Chaetocin also inhibited tumor growth in CRC xenograft models. In all, our study reveals that chaetocin induces CRC cell apoptosis, irrelevant to 5-FU sensitivity, by causing ROS accumulation and activating JNK/c-Jun, and enhances macrophages phagocytosis, which suggests chaetocin as a candidate for CRC chemotherapy.
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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 ╳
