1222800-79-4|ML324|ML324|MFCD28053518-范德生物科技公司

ML324

NMR下载 COA and HPLC MSDS下载
names：
ML324
CAS号：
1222800-79-4
MDL Number： MFCD28053518
MF(分子式)： C21H23N3O2 MW(分子量)： 349.43
EINECS: Reaxys Number:
Pubchem ID:44143209 Brand:BIOFOUNT

ML324(1222800-79-4)是一种有效的JMJD2脱甲基酶抑制剂，具有证明的抗病毒活性。IC50值：920 nM（JMJD2E）[1]；目标：JMJD2脱甲基酶抑制剂ML324是一种探针分子，对JMJD2E表现出亚微摩尔的抑制活性（体外），并具有出色的体外作用ADME属性。与以前报道的JMJD蛋白抑制剂相反，ML324显示出极好的细胞通透性，为进行JMJD2酶的基于细胞的更广泛研究提供了机会。此外，ML324通过抑制病毒IE基因表达，对单纯疱疹病毒（HSV）和人巨细胞病毒（hCMV）感染均显示出有效的抗病毒活性。ML324即使在高MOI时也能抑制HSV斑块的形成，并在潜伏感染小鼠的小鼠神经节外植体模型中阻止HSV-1的再激活。

货品编码	规格	纯度	价格 (¥)	现价(¥)	特价(¥)	库存描述	数量	总计 (¥)
HCC336053-1mg	1mg	97%	¥ 665.00	¥ 665.00		4-7周	- +	¥ 0.00

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中文别名	ML324(1222800-79-4);N-(3-(二甲氨基)丙基)-4-(8-羟基喹啉-6-基)苯甲酰胺;JMJD2去甲基酶抑制剂(ML324);
英文别名	ML324(1222800-79-4);ML-324；ML 324；ML324; CID-44143209；CID 44143209；CID44143209;ML243;N-[3-(Dimethylamino)propyl]-4-(8-hydroxy-6-quinolinyl)benzamide;NCGC00183808-01;ML324(CID-44143209);CS-2198;ML-324;ML324;ML 324;
CAS号	1222800-79-4
Inchi	InChI=1S/C21H23N3O2/c1-24(2)12-4-11-23-21(26)16-8-6-15(7-9-16)18-13-17-5-3-10-22-20(17)19(25)14-18/h3,5-10,13-14,25H,4,11-12H2,1-2H3,(H,23,26)
InchiKey	QDBVSOZTVKXUES-UHFFFAOYSA-N
分子式 Formula	C21H23N3O2
分子量 Molecular Weight	349.43
溶解度Solubility	生物体外In Vitro:DMSO溶解度≥ 33 mg/mL(94.44 mM)*"≥" means soluble可溶, but saturation unknown溶解度未知.
性状	白色至浅棕色固体粉末
储藏条件 Storage conditions	2-8°C，Refrigerator

ML324(1222800-79-4)实验注意事项：
1.实验前需戴好防护眼镜，穿戴防护服和口罩，佩戴手套，避免与皮肤接触。
2.实验过程中如遇到有毒或者刺激性物质及有害物质产生，必要时实验操作需要手套箱内完成以免对实验人员造成伤害
3.实验后产生的废弃物需分类存储，并交于专业生物废气物处理公司处理，以免造成环境污染Experimental considerations:
1. Wear protective glasses, protective clothing and masks, gloves, and avoid contact with the skin during the experiment.
2. The waste generated after the experiment needs to be stored separately, and handed over to a professional biological waste gas treatment company to avoid environmental pollution.

Tags:ML324试剂,ML324杂质,ML324合成,ML324中间体,ML324密度,ML324溶解度,ML324旋光度,ML324闪点,ML324购买,

产品说明	ML324(1222800-79-4)可以作为药物杂质对照品以及生物医药类试剂。
Introduction	ML324(1222800-79-4) can be used as a reference substance for drug impurities and reagents，only for research.
Application1	ML324是JMJD2去甲基酶抑制剂，被证实有抗病毒作用。
Application2	ML324是有效的JMJD2脱甲基酶抑制剂，在减少单纯疱疹病毒（HSV）IE基因表达中非常有效。ML324在潜在感染的小鼠的感觉神经节中有效地阻止了病毒裂解感染和HSV-1的激活。
Application3

ML324(1222800-79-4)药理学：

※ML324是JMJD2去甲基酶抑制剂，被证实有抗病毒作用。

※ML324是有效的JMJD2脱甲基酶抑制剂，在减少单纯疱疹病毒（HSV）IE基因表达中非常有效。ML324在潜在感染的小鼠的感觉神经节中有效地阻止了病毒裂解感染和HSV-1的激活。

警示图
危险性	warning
危险性警示	急性毒性
安全声明	H303+H313+H333
安全防护	P264+P280+P305+P351+P338+P337+P313
备注	实验过程中防止吸入、食入，做好安全防护

ML324(1222800-79-4)危害标识：

象形图
信号	Warning
GHS危险说明	H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]
GHS危险说明	Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown.
防范说明代码	P264, P270, P301+P312, P330, and P501
防范说明代码	(The corresponding statement to each P-code can be found at the GHS Classification page.)

Rai G, et al. Discovery of ML324, a JMJD2 demethylase inhibitor with demonstrated antiviral activity.

Histone Lysine Demethylases of JMJD2 or KDM4 Family are Important Epigenetic Regulators in Reward Circuitry in the Etiopathology of Depression PMID 27711046; Neuropsychopharmacology : official publica

Inhibition of KDM4A activity as a strategy to suppress interleukin-6 production and attenuate colitis induction PMID 28511912; Clinical immunology (Orlando, Fla.) 2017 07; 180(?):120-127 Name matches:

Inhibition of the histone demethylase KDM4B leads to activation of KDM1A, attenuates bacterial-induced pro-inflammatory cytokine release, and reduces osteoclastogenesis PMID 29927684; Epigenetics 2018

ML324(1222800-79-4)参考文献：

1.Histone Lysine Demethylases of JMJD2 or KDM4 Family are Important Epigenetic Regulators in Reward Circuitry in the Etiopathology of Depression.
Pathak SS;Maitra S;Chakravarty S;Kumar A Neuropsychopharmacology. 2017 Mar;42(4):854-863. doi: 10.1038/npp.2016.231. Epub 2016 Oct 6.

Major depressive disorder (MDD) is debilitating mental illness and is one of the leading contributors to global burden of disease, but unfortunately newer and better drugs are not forthcoming. The reason is lack of complete understanding of molecular mechanisms underlying the development of this disorder. Recent research shows dysregulation in epigenetic regulatory mechanisms, particularly the transcriptionally repressive di- and tri-methylation of histone 3 lysine 9 (H3K9me2/me3) in nucleus accumbens (NAc), a critical region of the reward pathway involved in the development of anhedonia, the hallmark of depression. However, the role of histone lysine demethylases, which can remove methylation from H3K9, in particular Jumonji domain containing demethylases 2 or Jmjd2 family, has not been studied. Using social defeat stress-induced mouse model of depression, this study uncovered that transcripts of most of the Jmjd2 members were unchanged after 5 days of defeat during the onset of depression, but were downregulated after 10 days of defeat in full-blown depression. Blocking the Jumonji domain containing demethylases by chronic administration of inhibitors dimethyloxalylglycine (DMOG) and ML324 resulted in depression-like phenotype even in absence of stress exposure, which was associated with an increase in transcriptionally repressive epigenetic marks H3K9me2/me3 in NAc, causing altered neuroplastic changes as reported in NAc in depression models.

2.Inhibition of the histone demethylase KDM4B leads to activation of KDM1A, attenuates bacterial-induced pro-inflammatory cytokine release, and reduces osteoclastogenesis.
Kirkpatrick JE;Kirkwood KL;Woster PM Epigenetics. 2018;13(5):557-572. doi: 10.1080/15592294.2018.1481703. Epub 2018 Aug 7.

Periodontal disease (PD) afflicts 46% of Americans with no effective adjunctive therapies available. While most pharmacotherapy for PD targets bacteria, the host immune response is responsible for driving tissue damage and bone loss in severe disease. Herein, we establish that the histone demethylase KDM4B is a potential drug target for the treatment of PD. Immunohistochemical staining of diseased periodontal epithelium revealed an increased abundance of KDM4B that correlates with inflammation. In murine calvarial sections exposed to Aggregatibacter actinomycetemcomitans lipopolysaccharide (Aa-LPS), immunohistochemical staining revealed a significant increase in KDM4B protein expression. The 8-hydroxyquinoline ML324 is known to inhibit the related demethylase KDM4E in vitro, but has not been evaluated against any other targets. Our studies indicate that ML324 also inhibits KDM4B (IC50: 4.9 μM), and decreases the pro-inflammatory cytokine response to an Aa-LPS challenge in vitro. Our results suggest that KDM4B inhibition-induced immunosuppression works indirectly, requiring new protein synthesis. In addition, fluorescence-stained macrophages exhibited a significant decrease in global monomethyl histone 3 lysine 4 (H3K4me) levels following an Aa-LPS challenge that was prevented by KDM4B inhibition, suggesting this effect is produced through KDM1A-mediated demethylation of H3K4.

3.Inhibition of KDM4A activity as a strategy to suppress interleukin-6 production and attenuate colitis induction.
Ishiguro K;Watanabe O;Nakamura M;Yamamura T;Matsushita M;Goto H;Hirooka Y Clin Immunol. 2017 Jul;180:120-127. doi: 10.1016/j.clim.2017.05.014. Epub 2017 May 13.

4-Chloro-7-nitro-2,1,3-benzoxadiazole (NBD-Cl) functions as a hapten and fluoresces upon binding to proteins. Therefore, fluorescence visualization of hapten-proteins is a feature of the colitis induced by NBD-Cl. Using this colitis model, we located activated fibroblasts in the vicinity of hapten-proteins upon colitis induction and observed interleukin (IL)-6 production in the activated fibroblasts. We screened herbal ingredients using primary fibroblasts stimulated with tumor necrosis factor α (TNF-α) and found the suppressive action of Atractylodin on IL-6 production. Under TNF-α stimulation, Atractylodin induced the tri-methylation of histone H3 at lysine residue 9, which impaired the binding between NF-κB and the IL-6 promoter on the genomic DNA. Atractylodin inhibited KDM4A but not KDM6A activity. Atractylodin administration attenuated colitis induction. The KDM4A inhibitor ML324 showed similar actions on IL-6 production and colitis induction. We propose the inhibition of KDM4A activity as a strategy to suppress IL-6 production and attenuate colitis induction.

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