Page last updated: 2024-12-11

1h-pyrrole-2,5-dione, 3-(1-methyl-1h-indol-3-yl)-4-(1-methyl-6-nitro-1h-indol-3-yl)-

Description Research Excerpts Clinical Trials Roles Classes Pathways Study Profile Bioassays Related Drugs Related Conditions Protein Interactions Research Growth Market Indicators

Description

You're describing a specific chemical compound with a rather complex name. Let's break it down and understand its potential research significance:

**1. The Core Structure:**

* **1H-pyrrole-2,5-dione:** This is the base structure. It's a heterocyclic compound containing a five-membered ring with one nitrogen atom (pyrrole) and two carbonyl groups (dione) at positions 2 and 5. This structure is often called a **succinimide**.
* **3-(1-methyl-1H-indol-3-yl)-4-(1-methyl-6-nitro-1H-indol-3-yl)-:** This part tells us that the succinimide ring is substituted with two indole groups.
* **Indole:** A bicyclic aromatic ring system containing a benzene ring fused to a pyrrole ring.
* **1-methyl-1H-indol-3-yl:** This signifies that an indole ring has a methyl group (CH3) attached to its nitrogen atom (position 1) and another substituent (in this case, it's attached to position 3).
* **1-methyl-6-nitro-1H-indol-3-yl:** Similar to the previous, but this indole has a nitro group (NO2) at position 6.

**2. Significance in Research:**

This compound, with its intricate structure, could be important for research in various areas:

* **Medicinal Chemistry:** The presence of indole rings, often found in naturally occurring bioactive molecules, suggests potential for pharmacological activity. This compound could be investigated as a potential drug lead for conditions involving inflammation, cancer, or neurological disorders.
* **Organic Chemistry:** This compound could be used as a building block for synthesizing novel organic compounds. The unique structural features could lead to the development of new materials with interesting properties.
* **Materials Science:** The presence of aromatic rings and potential for intermolecular interactions could lead to applications in materials science, such as the development of new organic semiconductors or conducting polymers.

**3. Further Investigation:**

To understand the true importance of this specific compound, more research is needed. Researchers would typically conduct experiments to determine:

* **Biological activity:** Does the compound have any therapeutic potential? Does it interact with specific receptors or enzymes?
* **Chemical properties:** How does the compound behave under different conditions? What are its solubility, stability, and reactivity?
* **Synthetic route:** How can the compound be efficiently synthesized in the lab?

**Important Note:** The name of this compound might be a shortened version or a specific nomenclature used in a particular research context. It's always best to consult the original scientific publication or source where you encountered this compound for complete and accurate information.

1H-pyrrole-2,5-dione, 3-(1-methyl-1H-indol-3-yl)-4-(1-methyl-6-nitro-1H-indol-3-yl)-: structure in first source [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

Cross-References

ID SourceID
PubMed CID5327686
CHEMBL ID52885
SCHEMBL ID608128
MeSH IDM0578177

Synonyms (30)

Synonym
3-(1-methyl-1h-indol-3-yl)-4-(1-methyl-6-nitro-1h-indol-3-yl)-2,5-dihydro-1h-pyrrole-2,5-dione
bisindolylmaleimide deriv. 44
bdbm2622
mkc-1
ro-31-7453
CHEMBL52885
ro 31-7453
mkc 1
3-(1-methylindol-3-yl)-4-(1-methyl-6-nitroindol-3-yl)pyrrole-2,5-dione
dnz11vpy7q ,
unii-dnz11vpy7q
1h-pyrrole-2,5-dione, 3-(1-methyl-1h-indol-3-yl)-4-(1-methyl-6-nitro-1h-indol-3-yl)-
r 440
125313-92-0
SCHEMBL608128
mkc 1 [who-dd]
OVSKGTONMLKNPZ-UHFFFAOYSA-N
3-(1-methyl-3-indolyl)-4-(1-methyl-6-nitro-3-indolyl)-1h-pyrrole-2,5-dione
m-kc1
3-(1-methyl-1h-indol-3-yl)-4-(1-methyl-6-nitro-1h-indol-3-yl)-1h-pyrrole-2,5-dione ,
DTXSID60154735
AKOS030228212
HY-13691
FT-0769873
DB05608
r 440; ro 31-7453
SB16541
Q27276500
AS-77693
CS-0007705

Research Excerpts

Pharmacokinetics

ExcerptReferenceRelevance
" Pharmacokinetic analysis showed rapid absorption and metabolism."( A phase I clinical and pharmacokinetic study of Ro 31-7453 given as a 7- or 14-day oral twice daily schedule every 4 weeks in patients with solid tumors.
Bissett, D; Breimer, L; Campbell, S; Cassidy, J; DeMario, M; Ritland, S; Salazar, R; Twelves, C; Zhi, J, 2004
)
0.32
" This regimen is convenient, well tolerated, and has a favorable pharmacokinetic profile."( A phase I clinical and pharmacokinetic study of Ro 31-7453 given as a 7- or 14-day oral twice daily schedule every 4 weeks in patients with solid tumors.
Bissett, D; Breimer, L; Campbell, S; Cassidy, J; DeMario, M; Ritland, S; Salazar, R; Twelves, C; Zhi, J, 2004
)
0.32
" The PK of the parent compound and major metabolites were apparently linear, with a half-life of approximately 9 hours and a maximum concentration of approximately 4 hours."( Phase I and pharmacokinetic study of the novel oral cell-cycle inhibitor Ro 31-7453 in patients with advanced solid tumors.
Aghajanian, C; Bienvenu, B; Breimer, L; Chang, C; DeMario, M; Dupont, J; Ng, K; Passe, S; Perkell, C; Pezzulli, S; Sabbatini, P; Soignet, SL; Spriggs, D; Vongphrachanh, P; Zhi, J, 2004
)
0.32

Bioavailability

ExcerptReferenceRelevance
"Cell membrane permeability is an important determinant for oral absorption and bioavailability of a drug molecule."( Highly predictive and interpretable models for PAMPA permeability.
Jadhav, A; Kerns, E; Nguyen, K; Shah, P; Sun, H; Xu, X; Yan, Z; Yu, KR, 2017
)
0.46

Dosage Studied

ExcerptRelevanceReference
" Clinical studies demonstrated modest antitumor activity using intermittent dosing schedule, however additional preclinical data suggested continuous dosing could be efficacious with additional effects against the mTor/AKT pathway."( Phase I study of continuous MKC-1 in patients with advanced or metastatic solid malignancies using the modified Time-to-Event Continual Reassessment Method (TITE-CRM) dose escalation design.
Arnott, J; Bailey, H; Chappell, R; Eickhoff, J; Liu, G; Schelman, W; Sidor, C; Tevaarwerk, A; Wilding, G, 2012
)
0.38
" MKC-1 was dosed twice daily, continuously in 28-day cycles."( Phase I study of continuous MKC-1 in patients with advanced or metastatic solid malignancies using the modified Time-to-Event Continual Reassessment Method (TITE-CRM) dose escalation design.
Arnott, J; Bailey, H; Chappell, R; Eickhoff, J; Liu, G; Schelman, W; Sidor, C; Tevaarwerk, A; Wilding, G, 2012
)
0.38
" Patients 1-3 received 120 mg/d of MKC-1; patients 4-24 were dosed per the TITE-CRM algorithm: 150 mg [n = 1], 180 [2], 200 [1], 230 [1], 260 [5], 290 [6], 320 [5]."( Phase I study of continuous MKC-1 in patients with advanced or metastatic solid malignancies using the modified Time-to-Event Continual Reassessment Method (TITE-CRM) dose escalation design.
Arnott, J; Bailey, H; Chappell, R; Eickhoff, J; Liu, G; Schelman, W; Sidor, C; Tevaarwerk, A; Wilding, G, 2012
)
0.38
" Dose escalation stopped at 320 mg/d, and this is the MTD as defined by the CRM dose escalation algorithm; this cumulative dose/cycle exceeds that determined from intermittent dosing studies."( Phase I study of continuous MKC-1 in patients with advanced or metastatic solid malignancies using the modified Time-to-Event Continual Reassessment Method (TITE-CRM) dose escalation design.
Arnott, J; Bailey, H; Chappell, R; Eickhoff, J; Liu, G; Schelman, W; Sidor, C; Tevaarwerk, A; Wilding, G, 2012
)
0.38
" MKC-1 was administered orally, twice daily, initially at 100 mg/m(2) dosing for 14 consecutive days of a 28-day cycle."( A phase 2 study of oral MKC-1, an inhibitor of importin-β, tubulin, and the mTOR pathway in patients with unresectable or metastatic pancreatic cancer.
Abrams, TA; Arnott, J; Blaszkowsky, LS; Clark, JW; Enzinger, PC; Faris, JE; Hezel, AF; Kwak, EL; Ng, K; Ryan, DP; Wolpin, BM; Zheng, H, 2012
)
0.38
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Protein Targets (4)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
PPM1D proteinHomo sapiens (human)Potency13.13730.00529.466132.9993AID1347411
Interferon betaHomo sapiens (human)Potency13.13730.00339.158239.8107AID1347411
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Inhibition Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Protein kinase C gamma typeRattus norvegicus (Norway rat)IC50 (µMol)1.10000.00000.26401.1000AID165104
Protein kinase C beta typeRattus norvegicus (Norway rat)IC50 (µMol)1.10000.00000.21641.1000AID1795401
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (30)

Processvia Protein(s)Taxonomy
cell surface receptor signaling pathway via JAK-STATInterferon betaHomo sapiens (human)
response to exogenous dsRNAInterferon betaHomo sapiens (human)
B cell activation involved in immune responseInterferon betaHomo sapiens (human)
cell surface receptor signaling pathwayInterferon betaHomo sapiens (human)
cell surface receptor signaling pathway via JAK-STATInterferon betaHomo sapiens (human)
response to virusInterferon betaHomo sapiens (human)
positive regulation of autophagyInterferon betaHomo sapiens (human)
cytokine-mediated signaling pathwayInterferon betaHomo sapiens (human)
natural killer cell activationInterferon betaHomo sapiens (human)
positive regulation of peptidyl-serine phosphorylation of STAT proteinInterferon betaHomo sapiens (human)
cellular response to interferon-betaInterferon betaHomo sapiens (human)
B cell proliferationInterferon betaHomo sapiens (human)
negative regulation of viral genome replicationInterferon betaHomo sapiens (human)
innate immune responseInterferon betaHomo sapiens (human)
positive regulation of innate immune responseInterferon betaHomo sapiens (human)
regulation of MHC class I biosynthetic processInterferon betaHomo sapiens (human)
negative regulation of T cell differentiationInterferon betaHomo sapiens (human)
positive regulation of transcription by RNA polymerase IIInterferon betaHomo sapiens (human)
defense response to virusInterferon betaHomo sapiens (human)
type I interferon-mediated signaling pathwayInterferon betaHomo sapiens (human)
neuron cellular homeostasisInterferon betaHomo sapiens (human)
cellular response to exogenous dsRNAInterferon betaHomo sapiens (human)
cellular response to virusInterferon betaHomo sapiens (human)
negative regulation of Lewy body formationInterferon betaHomo sapiens (human)
negative regulation of T-helper 2 cell cytokine productionInterferon betaHomo sapiens (human)
positive regulation of apoptotic signaling pathwayInterferon betaHomo sapiens (human)
response to exogenous dsRNAInterferon betaHomo sapiens (human)
B cell differentiationInterferon betaHomo sapiens (human)
natural killer cell activation involved in immune responseInterferon betaHomo sapiens (human)
adaptive immune responseInterferon betaHomo sapiens (human)
T cell activation involved in immune responseInterferon betaHomo sapiens (human)
humoral immune responseInterferon betaHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (5)

Processvia Protein(s)Taxonomy
cytokine activityInterferon betaHomo sapiens (human)
cytokine receptor bindingInterferon betaHomo sapiens (human)
type I interferon receptor bindingInterferon betaHomo sapiens (human)
protein bindingInterferon betaHomo sapiens (human)
chloramphenicol O-acetyltransferase activityInterferon betaHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (2)

Processvia Protein(s)Taxonomy
extracellular spaceInterferon betaHomo sapiens (human)
extracellular regionInterferon betaHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (6)

Assay IDTitleYearJournalArticle
AID1508591NCATS Rat Liver Microsome Stability Profiling2020Scientific reports, 11-26, Volume: 10, Issue:1
Retrospective assessment of rat liver microsomal stability at NCATS: data and QSAR models.
AID1347411qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Mechanism Interrogation Plate v5.0 (MIPE) Libary2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1508612NCATS Parallel Artificial Membrane Permeability Assay (PAMPA) Profiling2017Bioorganic & medicinal chemistry, 02-01, Volume: 25, Issue:3
Highly predictive and interpretable models for PAMPA permeability.
AID1645848NCATS Kinetic Aqueous Solubility Profiling2019Bioorganic & medicinal chemistry, 07-15, Volume: 27, Issue:14
Predictive models of aqueous solubility of organic compounds built on A large dataset of high integrity.
AID165104Inhibition of rat brain protein kinase C (PKC) with ATP and histone as substrates1992Journal of medicinal chemistry, Jan, Volume: 35, Issue:1
Inhibitors of protein kinase C. 1. 2,3-Bisarylmaleimides.
AID1795401PKC assay from Article 10.1021/jm00079a024: \\Inhibitors of protein kinase C. 1. 2,3-Bisarylmaleimides.\\1992Journal of medicinal chemistry, Jan, Volume: 35, Issue:1
Inhibitors of protein kinase C. 1. 2,3-Bisarylmaleimides.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (10)

TimeframeStudies, This Drug (%)All Drugs %
pre-19900 (0.00)18.7374
1990's1 (10.00)18.2507
2000's2 (20.00)29.6817
2010's5 (50.00)24.3611
2020's2 (20.00)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 12.27

According to the monthly volume, diversity, and competition of internet searches for this compound, as well the volume and growth of publications, there is estimated to be weak demand-to-supply ratio for research on this compound.

MetricThis Compound (vs All)
Research Demand Index12.27 (24.57)
Research Supply Index2.71 (2.92)
Research Growth Index4.97 (4.65)
Search Engine Demand Index0.00 (26.88)
Search Engine Supply Index0.00 (0.95)

This Compound (12.27)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials4 (40.00%)5.53%
Reviews0 (0.00%)6.00%
Case Studies0 (0.00%)4.05%
Observational0 (0.00%)0.25%
Other6 (60.00%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]