Indole-3-carbinol
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| Category | Enzyme inhibitors |
| Catalog number | BBF-04515 |
| CAS | 700-06-1 |
| Molecular Weight | 147.17 |
| Molecular Formula | C9H9NO |
| Purity | 98% |
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Description
Indole-3-carbinol is an inhibitor of cell growth via suppressing incorporation of [3H]thymidine, triggering G1 cell cycle arrest and downregulation of cyclin-dependent kinase 6 (CDK6) expression. It exhibits anticancer activity by inhibition of NF-κB and Akt signaling pathways. Nutritional supplement in health care products.
Specification
| Related CAS | 123334-15-6 (hydrate) |
| Synonyms | 3-Indolemethanol; (1H-Indol-3-yl)methanol; Indole-3-methanol; Indol-3-yl-methanol; 3-Hydroxymethylindole; I3C; Indinol |
| Storage | Store at -20°C under inert atmosphere |
| IUPAC Name | 1H-indol-3-ylmEthanol |
| Canonical SMILES | C1=CC=C2C(=C1)C(=CN2)CO |
| InChI | InChI=1S/C9H9NO/c11-6-7-5-10-9-4-2-1-3-8(7)9/h1-5,10-11H,6H2 |
| InChI Key | IVYPNXXAYMYVSP-UHFFFAOYSA-N |
Properties
| Appearance | Off-white to Pale Orange Solid |
| Antibiotic Activity Spectrum | Neoplastics (Tumor) |
| Boiling Point | 360.6°C at 760 mmHg |
| Melting Point | 96-99°C |
| Density | 1.272 g/cm3 |
| Solubility | Slightly soluble in DMSO, Methanol |
Reference Reading
1.Phenethyl isothiocyanate and indole-3-carbinol from cruciferous vegetables, but not furanocoumarins from apiaceous vegetables, reduced PhIP-induced DNA adducts in Wistar rats.
Kim JK1, Gallaher DD2, Chen C2, Gallaher CM2, Yao D2, Trudo SP1. Mol Nutr Food Res. 2016 May 2. doi: 10.1002/mnfr.201500790. [Epub ahead of print]
SCOPE: We previously showed that apiaceous but not cruciferous vegetables reduced DNA adducts formed by 2-amino-1-methyl-6-phenylimidazo[4, 5-b]pyridine (PhIP) in rats. Here, we report the effects of the putative chemopreventive phytochemicals from these vegetables on PhIP metabolism and DNA adduct formation.
2.Cooperative antiproliferative signaling by aspirin and indole-3-carbinol targets microphthalmia-associated transcription factor gene expression and promoter activity in human melanoma cells.
Poindexter KM1, Matthew S1, Aronchik I1, Firestone GL2. Cell Biol Toxicol. 2016 Apr;32(2):103-19. doi: 10.1007/s10565-016-9321-5. Epub 2016 Apr 7.
Antiproliferative signaling of combinations of the nonsteroidal anti-inflammatory drug acetylsalicylic acid (aspirin) and indole-3-carbinol (I3C), a natural indolecarbinol compound derived from cruciferous vegetables, was investigated in human melanoma cells. Melanoma cell lines with distinct mutational profiles were sensitive to different extents to the antiproliferative response of aspirin, with oncogenic BRAF-expressing G361 cells and wild-type BRAF-expressing SK-MEL-30 cells being the most responsive. I3C triggered a strong proliferative arrest of G361 melanoma cells and caused only a modest decrease in the proliferation of SK-MEL-30 cells. In both cell lines, combinations of aspirin and I3C cooperatively arrested cell proliferation and induced a G1 cell cycle arrest, and nearly ablated protein and transcript levels of the melanocyte master regulator microphthalmia-associated transcription factor isoform M (MITF-M). In melanoma cells transfected with a -333/+120-bp MITF-M promoter-luciferase reporter plasmid, treatment with aspirin and I3C cooperatively disrupted MITF-M promoter activity, which accounted for the loss of MITF-M gene products.
3.Inhibition of oncogenic BRAF activity by indole-3-carbinol disrupts microphthalmia-associated transcription factor expression and arrests melanoma cell proliferation.
Kundu A1, Quirit JG1, Khouri MG1, Firestone GL1. Mol Carcinog. 2016 Feb 15. doi: 10.1002/mc.22472. [Epub ahead of print]
Indole-3-carbinol (I3C), an anti-cancer phytochemical derived from cruciferous vegetables, strongly inhibited proliferation and down-regulated protein levels of the melanocyte master regulator micropthalmia-associated transcription factor (MITF-M) in oncogenic BRAF-V600E expressing melanoma cells in culture as well as in vivo in tumor xenografted athymic nude mice. In contrast, wild type BRAF-expressing melanoma cells remained relatively insensitive to I3C anti-proliferative signaling. In BRAF-V600E-expressing melanoma cells, I3C treatment inhibited phosphorylation of MEK and ERK/MAPK, the down stream effectors of BRAF. The I3C anti-proliferative arrest was concomitant with the down-regulation of MITF-M transcripts and promoter activity, loss of endogenous BRN-2 binding to the MITF-M promoter, and was strongly attenuated by expression of exogenous MITF-M. Importantly, in vitro kinase assays using immunoprecipitated BRAF-V600E and wild type BRAF demonstrated that I3C selectively inhibited the enzymatic activity of the oncogenic BRAF-V600E but not of the wild type protein.
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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 ╳
