Indoximod - CAS 110117-83-4
Catalog number: 110117-83-4
Category: Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
Molecular Weight:
A methylated tryptophan with immune checkpoint inhibitory activity. Indoximod inhibits the enzyme indoleamine 2,3-dioxygenase (IDO), which degrades the essential amino acid tryptophan, and may increase or maintain tryptophan levels important to T cell function. Tryptophan depletion is associated with immunosuppression involving T cell arrest and anergy.
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Brife Description:
A methylated tryptophan Indoximod inhibits the enzyme IDO with immune checkpoint inhibitory activity.
> 98%
Off-White Solid
Indoximod; NLG8189; NLG 8189; NLG-8189; D-1MT; 1-methyl-D-tryptophan.
Soluble in DMSO, not in water
Dry, dark and at 0 - 4 C for short term (days to weeks) or -20 C for long term (months to years).
Quality Standard:
Shelf Life:
>2 years if stored properly
Melting Point:
247-250°C (dec.)
Canonical SMILES:
Current Developer:
National Cancer Institute (USA); NewLink Genetics Corporation; University of Minnesota
1.A Phase I study of indoximod in patients with advanced malignancies.
Soliman HH1, Minton SE1, Han HS1, Ismail-Khan R1, Neuger A1, Khambati F1, Noyes D1, Lush R1, Chiappori AA1, Roberts JD2, Link C3, Vahanian NN3, Mautino M3, Streicher H4, Sullivan DM1, Antonia SJ1. Oncotarget. 2016 Mar 20. doi: 10.18632/oncotarget.8216. [Epub ahead of print]
PURPOSE: Indoximod is an oral inhibitor of the indoleamine 2,3-dioxygenase pathway, which causes tumor-mediated immunosuppression. Primary endpoints were maximum tolerated dose (MTD) and toxicity for indoximod in patients with advanced solid tumors. Secondary endpoints included response rates, pharmacokinetics, and immune correlates.
2.An untargeted global metabolomic analysis reveals the biochemical changes underlying basal resistance and priming in Solanum lycopersicum, and identifies 1-methyltryptophan as a metabolite involved in plant responses to Botrytis cinerea and Pseudomonas sy
Camañes G1, Scalschi L1, Vicedo B1, González-Bosch C2, García-Agustín P1. Plant J. 2015 Oct;84(1):125-39. doi: 10.1111/tpj.12964.
In this study, we have used untargeted global metabolomic analysis to determine and compare the chemical nature of the metabolites altered during the infection of tomato plants (cv. Ailsa Craig) with Botrytis cinerea (Bot) or Pseudomonas syringae pv. tomato DC3000 (Pst), pathogens that have different invasion mechanisms and lifestyles. We also obtained the metabolome of tomato plants primed using the natural resistance inducer hexanoic acid and then infected with these pathogens. By contrasting the metabolomic profiles of infected, primed, and primed + infected plants, we determined not only the processes or components related directly to plant defense responses, but also inferred the metabolic mechanisms by which pathogen resistance is primed. The data show that basal resistance and hexanoic acid-induced resistance to Bot and Pst are associated with a marked metabolic reprogramming. This includes significant changes in amino acids, sugars and free fatty acids, and in primary and secondary metabolism.
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