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Indirubin

$43

  • Brand : BIOFRON

  • Catalogue Number : BF-I1001

  • Specification : 98%

  • CAS number : 479-41-4

  • Formula : C16H10N2O2

  • Molecular Weight : 262.26

  • PUBCHEM ID : 10177

  • Volume : 20mg

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Catalogue Number

BF-I1001

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

262.26

Appearance

Red crystalline powder

Botanical Source

Isatis tinctoria

Structure Type

Alkaloids

Category

Standards;Natural Pytochemical;API

SMILES

C1=CC=C2C(=C1)C(=C(N2)O)C3=NC4=CC=CC=C4C3=O

Synonyms

5-24-08-0​0507/Indirubin/(3Z)-3-(3-Oxo-1,3-dihydro-2H-indol-2-ylidene)-1,3-dihydro-2H-indol-2-one/Indigo Red/2-ylidene)-1,3-dihydro/COUROUPITINE B/[2,3'-Biindolinylidene]-2',3-dione/INDIGOPURPURIN/2H-Indol-2-one, 3-(1,3-dihydro-3-oxo-2H-indol-2-ylidene)-1,3-dihydro-, (3Z)-

IUPAC Name

2-(2-hydroxy-1H-indol-3-yl)indol-3-one

Density

1.4±0.1 g/cm3

Solubility

Methanol; DMSO

Flash Point

207.0±28.9 °C

Boiling Point

496.6±45.0 °C at 760 mmHg

Melting Point

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2933990000

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:479-41-4) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

31014934

Abstract

Indirubin, a traditional Chinese medicine, is currently used to treat certain autoimmune diseases such as primary immune thrombocytopenia (ITP) in clinics. However, the effects of indirubin on expression of related genes in peripheral blood mononuclear cells (PBMCs) from ITP patients have not been investigated. In the present study, PBMCs were isolated from 19 adult patients with well-characterized active ITP and 20 healthy controls (HCs) and then treated with increasing concentrations of indirubin. The mRNA expression levels of thrombopoietin receptor (MPL), GATA binding protein 3 (GATA3), DNA methyltransferase 3B (DNMT3B), interleukin-6 (IL6), tumor necrosis factor (TNF), and interferon gamma (IFN-γ) were determined by quantitative real-time polymerase chain reaction (PCR). We found that indirubin had no cytotoxic effect on PBMC viability. Significantly lower MPL (p < 0.05) and GATA3 (p < 0.05) expression together with markedly higher IL6 (p < 0.05), TNF (p < 0.0001), and IFN-γ (p < 0.001) mRNA levels were observed in ITP patients compared with HCs. Notably, indirubin significantly enhanced MPL expression and inhibited TNF expression in PBMCs from ITP patients (p < 0.05). In summary, indirubin may play a direct role in thrombopoiesis by activating cellular MPL and normalizing TNF expression to suppress inflammation in ITP. This study may thus improve our understanding of indirubin and provide important information for optimizing therapeutic strategies for ITP patients.

Copyright © 2019. Published by Elsevier Inc.

Title

Indirubin regulates MPL and TNF expression in peripheral blood mononuclear cells from patients with primary immune thrombocytopenia.

Author

Shao K1, Wang T2, Li T3, Zhang A4, Cai M5, Zhao G3, Fu Q3, Wang Q6, Liu X5, Hou M7.

Publish date

2019 May

PMID

30909944

Abstract

BACKGROUND:
The introduction of imatinib revolutionized the treatment of chronic myeloid leukaemia (CML), substantially extending patient survival. However, imatinib resistance is currently a clinical problem for CML. It is very importantto find a strategy to inhibit imatinib resistance.

METHODS:
(1) We Identified indirubin and its derivatives and predicted its putative targets; (2) We downloaded data of the gene chip GSE2810 from the Gene Expression Omnibus (GEO) database and performed GEO2R analysis to obtain differentially expressed genes (DEGs); and (3) we constructed a P-P network of putative targets and DEGs to explore the mechanisms of action and to verify the results of molecular docking.

RESULT:
We Identified a total of 42 small-molecule compounds, of which 15 affected 11 putative targets, indicating the potential to inhibit imatinib resistance; the results of molecular docking verified these results. Six biomarkers of imatinib resistance were characterised by analysing DEGs.

CONCLUSION:
The 15 small molecule compounds inhibited imatinib resistance through the cytokine-cytokine receptor signalling pathway, the JAK-stat pathway, and the NF-KB signalling pathway. Indirubin and its derivatives may be new drugsthat can combat imatinib resistance.

KEYWORDS

Derivatives; Drug target prediction; Gene microarray analysis; Imatinib resistance; Indirubin; Protein network construction

Title

Deciphering the mechanism of Indirubin and its derivatives in the inhibition of Imatinib resistance using a "drug target prediction-gene microarray analysis-protein network construction" strategy.

Author

Li H1, Liu L1,2, Zhuang J2, Liu C1, Zhou C3, Yang J3, Gao C1, Liu G3, Sun C4,5.

Publish date

2019 Mar 25

PMID

30866411

Abstract

Cutaneous T-cell lymphoma (CTCL) may develop a highly malignant phenotype in its late phase, and patients may profit from innovative therapies. The plant extract indirubin and its chemical derivatives represent new and promising antitumor strategies. This first report on the effects of an indirubin derivative in CTCL cells shows a strong decrease of cell proliferation and cell viability as well as an induction of apoptosis, suggesting indirubin derivatives for therapy of CTCL. As concerning the mode of activity, the indirubin derivative DKP-071 activated the extrinsic apoptosis cascade via caspase-8 and caspase-3 through downregulation of the caspase antagonistic proteins c-FLIP and XIAP. Importantly, a strong increase of reactive oxygen species (ROS) was observed as an immediate early effect in response to DKP-071 treatment. The use of antioxidative pre-treatment proved the decisive role of ROS, which turned out upstream of all other proapoptotic effects monitored. Thus, reactive oxygen species appear as a highly active proapoptotic pathway in CTCL, which may be promising for therapeutic intervention. This pathway can be efficiently activated by an indirubin derivative.

KEYWORDS

CTCL; XIAP; apoptosis; c-FLIP; cell viability

Title

Key Role of Reactive Oxygen Species (ROS) in Indirubin Derivative-Induced Cell Death in Cutaneous T-Cell Lymphoma Cells.

Author

Soltan MY1,2, Sumarni U3, Assaf C4,5, Langer P6,7, Reidel U8, Eberle J9.

Publish date

2019 Mar 7


Description :

Indirubin(Couroupitine B) is a purple 3,2- bisindole and a stable isomer of indigo isolated from Indigo naturalis (Apiaceae); anti-inflammatory and anticancer activities.IC50 value:Target:in vitro: The activation of EGF receptor, known to be highly expressed in psoriatic lesions, was inhibited by indigo naturalis or indirubin. The cell proliferation and CDC25B expression of epidermal keratinocytes were induced by EGF alone and confirmed to be inhibited by indigo naturalis or indirubin [2]. indirubin inhibited prostate tumor growth through inhibiting tumor angiogenesis. indirubin inhibited angiogenesis in vivo. We also showed the inhibition activity of indirubin in endothelial cell migration, tube formation and cell survival in vitro [3].in vivo: Indirubin treatment suppressed skin inflammation in DNCB-exposed mice. The skin lesions were significantly thinner in the Indirubin-treated group than in untreated controls, and the hyperkeratosis disappeared. Indirubin reduced the total serum IgE level and cytokines production. In addition, it normalized NF-κB, IκB-α and MAP kinase expression [1]. Indirubin dose-dependently inhibited intersegmental vessel formation in zebrafish embryos. It also inhibited HUVEC proliferation by the induction of cellular apoptosis and cell-cycle arrest at the G0/G1 phase [4].