Gliocidin

  Cat. No.:  DC21715   Featured
Chemical Structure
62289-81-0
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More than 5000 active chemicals with high quality for research!
Field of application
Gliocidin is a nicotinamide-mimetic prodrug that targets glioblastoma. Gliocidin activity targets a de novo purine synthesis vulnerability in glioblastoma through indirect inhibition of inosine monophosphate dehydrogenase 2 (IMPDH2). IMPDH2 blockade reduces intracellular guanine nucleotide levels, causing nucleotide imbalance, replication stress and tumour cell death. Gliocidin is a prodrug that is anabolized into its tumoricidal metabolite, gliocidin–adenine dinucleotide (GAD), by the enzyme nicotinamide nucleotide adenylyltransferase 1 (NMNAT1) of the NAD+ salvage pathway. The cryo-electron microscopy structure of GAD together with IMPDH2 demonstrates its entry, deformation and blockade of the NAD+ pocket3. In vivo, gliocidin penetrates the blood–brain barrier and extends the survival of mice with orthotopic glioblastoma. The DNA alkylating agent temozolomide induces Nmnat1 expression, causing synergistic tumour cell killing and additional survival benefit in orthotopic patient-derived xenograft models. Gliocidin is a prodrug with the potential to improve the survival of patients with glioblastoma.
Cas No.: 62289-81-0
Chemical Name: N-(pyridin-3-yl)thiophene-2-carboxamide
Synonyms: SW106065;MPNST-IN-21
SMILES: O=C(NC1C=NC=CC=1)C2SC=CC=2
Formula: C10H8N2Os
M.Wt: 204.247
Purity: >98%
Sotrage: 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
Publication: Nature-20 November 2024 Gliocidin is a nicotinamide-mimetic prodrug that targets glioblastoma
Description: Gliocidin is a nicotinamide-mimetic prodrug that targets glioblastoma. Gliocidin activity targets a de novo purine synthesis vulnerability in glioblastoma through indirect inhibition of inosine monophosphate dehydrogenase 2 (IMPDH2). IMPDH2 blockade reduces intracellular guanine nucleotide levels, causing nucleotide imbalance, replication stress and tumour cell death. Gliocidin is a prodrug that is anabolized into its tumoricidal metabolite, gliocidin–adenine dinucleotide (GAD), by the enzyme nicotinamide nucleotide adenylyltransferase 1 (NMNAT1) of the NAD+ salvage pathway. The cryo-electron microscopy structure of GAD together with IMPDH2 demonstrates its entry, deformation and blockade of the NAD+ pocket3. In vivo, gliocidin penetrates the blood–brain barrier and extends the survival of mice with orthotopic glioblastoma. The DNA alkylating agent temozolomide induces Nmnat1 expression, causing synergistic tumour cell killing and additional survival benefit in orthotopic patient-derived xenograft models. Gliocidin is a prodrug with the potential to improve the survival of patients with glioblastoma.
References: Nature-20 November 2024 Gliocidin is a nicotinamide-mimetic prodrug that targets glioblastoma
MSDS
COA
LOT NO. DOWNLOAD
2018-0101
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