Lonidamine

製品コードS2610 バッチS261003

化学情報

	Synonyms	AF-1890, Diclondazolic Acid, DICA	Storage (From the date of receipt)	3 years -20°C powder 1 years -80°C in solvent
	化学式	C₁₅H₁₀Cl₂N₂O₂
	分子量	321.16	CAS No.	50264-69-2
Solubility (25°C)*	体外	DMSO	64 mg/mL (199.27 mM)
		Water	Insoluble
		Ethanol	Insoluble
* <1 mg/ml means slightly soluble or insoluble. * Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

溶剤液（一定の濃度）を調合する

生物活性

製品説明	Lonidamine is an orally administered small molecule hexokinase inactivator.
in vitro	Lonidamine reduces the oxygen consumption in both normal and neoplastic cells, while it increases the aerobic glycolysis of normal cells but inhibited that of tumor cells. ^[1] Lonidamine induces the permeabilization of ANT proteoliposomes in a cell-free system, yet has no effect on protein-free liposomes. Lonidamine adds to synthetic planar lipid bilayers containing ANT, eliciting ANT channel activities with clearly distinct conductance levels. ^[2] Lonidamine provokes a disruption of the mitochondrial transmembrane potential which precedes signs of nuclear apoptosis and cytolysis. Lonidamine causes the dissipation of the mitochondrial inner transmembrane potential and the release of apoptogenic factors capable of inducing nuclear apoptosis in vitro. ^[3] Lonidamine (50 mg/mL) induces apoptosis in adriamycin and nitrosourea-resistant cells (MCF-7 ADR(r) human breast cancer cell line, and LB9 glioblastoma multiform cell line), as demonstrated by sub-G1 peaks in DNA content histograms, condensation of nuclear chromatin, and internucleosomal DNA fragmentation. ^[4] Lonidamine has a stronger effect on glioblastoma cell proliferation and metabolism in vitro than did either agent used alone. ^[5]
in vivo	Lonidamine (160 mg/kg) combined with Diazepam is significantly more effective in reducing glioblastoma tumor growth than either drug alone in mice, this tumor growth retardation is maintained as long as treatment is given. ^[5]

製品説明

Lonidamine is an orally administered small molecule hexokinase inactivator.

in vitro

Lonidamine reduces the oxygen consumption in both normal and neoplastic cells, while it increases the aerobic glycolysis of normal cells but inhibited that of tumor cells. ^[1]

Lonidamine induces the permeabilization of ANT proteoliposomes in a cell-free system, yet has no effect on protein-free liposomes. Lonidamine adds to synthetic planar lipid bilayers containing ANT, eliciting ANT channel activities with clearly distinct conductance levels. ^[2]

Lonidamine provokes a disruption of the mitochondrial transmembrane potential which precedes signs of nuclear apoptosis and cytolysis. Lonidamine causes the dissipation of the mitochondrial inner transmembrane potential and the release of apoptogenic factors capable of inducing nuclear apoptosis in vitro. ^[3]

Lonidamine (50 mg/mL) induces apoptosis in adriamycin and nitrosourea-resistant cells (MCF-7 ADR(r) human breast cancer cell line, and LB9 glioblastoma multiform cell line), as demonstrated by sub-G1 peaks in DNA content histograms, condensation of nuclear chromatin, and internucleosomal DNA fragmentation. ^[4]

Lonidamine has a stronger effect on glioblastoma cell proliferation and metabolism in vitro than did either agent used alone. ^[5]

in vivo

Lonidamine (160 mg/kg) combined with Diazepam is significantly more effective in reducing glioblastoma tumor growth than either drug alone in mice, this tumor growth retardation is maintained as long as treatment is given. ^[5]

プロトコル(参考用のみ)

細胞アッセイ	細胞株	Klein sarcoma cells
	濃度	0.32 nM
	反応時間
	実験の流れ	Cells were treated with varying concentrations of Lonidamine.
動物実験	動物モデル	Female nu/nu mice
	投薬量	80 mg/kg
	投与方法	Tail vein

参考

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Selleckの高級品が、幾つかの出版された研究調査結果（以下を含む）で使われた：

Targeting tumor-intrinsic SLC16A3 to enhance anti-PD-1 efficacy via tumor immune microenvironment reprogramming [ Cancer Lett, 2024, 589:216824]	PubMed: 38522774
Targeting mitochondrial energetics reverses panobinostat- and marizomib-induced resistance in pediatric and adult high-grade gliomas [ Mol Oncol, 2023, 17(9):1821-1843]	PubMed: 37014128
Targeting mitochondrial energetics reverses panobinostat- and marizomib-induced resistance in pediatric and adult high-grade gliomas [ Mol Oncol, 2023, 17(9):1821-1843]	PubMed: 37014128
Metabolic Reprogramming by Ribitol Expands the Therapeutic Window of BETi JQ1 against Breast Cancer [ Cancers (Basel), 2023, 15(17)4356]	PubMed: 37686632
Metabolic Reprogramming by Ribitol Expands the Therapeutic Window of BETi JQ1 against Breast Cancer [ Cancers (Basel), 2023, 15(17)4356]	PubMed: 37686632
Microglial hexokinase 2 deficiency increases ATP generation through lipid metabolism leading to β-amyloid clearance [ Nat Metab, 2022, 4(10):1287-1305]	PubMed: 36203054
Deregulation and epigenetic modification of BCL2-family genes cause resistance to venetoclax in hematologic malignancies [ Blood, 2022, blood.2021014304]	PubMed: 35704690
Directly targeting ASC by lonidamine alleviates inflammasome-driven diseases [ J Neuroinflammation, 2022, 19(1):315]	PubMed: 36577999
Membrane-associated RING-CH protein (MARCH8) is a novel glycolysis repressor targeted by miR-32 in colorectal cancer [ J Transl Med, 2022, 20(1):402]	PubMed: 36064706
Hexokinase 2-mediated glycolysis promotes receptor activator of NF-κB ligand expression in Porphyromonas gingivalis lipopolysaccharide-treated osteoblasts [ J Periodontol, 2021, 10.1002/JPER.21-0227]	PubMed: 34585393

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人間や獣医の診断であるか治療的な使用のためにでない。

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