2. Epigenetics Apoptosis
  3. Histone Demethylase Apoptosis
  4. DC551040

DC551040 是一种口服有效和选择性的赖氨酸去甲基化酶 1 (LSD1) 抑制剂，对人源 LSD1 的 IC50 为 2.14 nM。DC551040 通过与 Trp552 形成 π-π 堆积作用、与 Phe538 形成极性相互作用、与 FAD 形成共价加合物的方式结合 LSD1，并破坏 LSD1-GFI1B-CoREST 复合物。DC551040 可诱导 H3K4me2 积累、细胞凋亡 (apoptosis) 与分化，激活 STAT5、NF-κB、AKT 以及 IL6-STAT3 通路，并上调 IL6 的表达。DC551040 可用于急性髓系白血病的相关研究。

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DC551040

DC551040 Chemical Structure

CAS No. : 2133291-32-2

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DC551040 相关抗体

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KDM1/LSD1 KDM2 KDM3 KDM4 KDM5 KDM6 KDM7

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

DC551040 is an orally active and selective lysine demethylase 1 (LSD1) inhibitor with a human IC50 of 2.14 nM. DC551040 binds to LSD1 via π-π stacking with Trp552, polar interactions with Phe538, and covalent adduct formation with FAD, and disrupts the LSD1-GFI1B-CoREST complex. DC551040 induces H3K4me2 accumulation, apoptosis, and cell differentiation, activates STAT5, NF-κB, AKT, and IL6-STAT3 pathways, and upregulates IL6 expression. DC551040 can be used for the research of acute myeloid leukemia[1].

IC50 & Target[1]

LSD1

2.14 nM (IC50)

体外研究
(In Vitro)

DC551040 (孵育 1 小时) 可强效抑制重组人源 LSD1 的酶活性，其 IC50 为 2.14 nM[1]。
DC551040 对重组人源 LSD1 表现出相较于重组人源 LSD2、MAO-A 及 MAO-B 的优异选择性[1]。
DC551040 (300 nM；1 小时预处理) 可不可逆地抑制重组人源 LSD1，因为稀释后酶活性无法恢复[1]。
DC551040 (50-250 nM；24 小时) 可破坏 MV-4-11 急性髓系白血病 (AML) 细胞中的 LSD1-GFI1B-CoREST 复合物[1]。
DC551040 (7 天) 可强效抑制 MV-4-11、Kasumi-1 和 HL-60 急性髓系白血病 (AML) 细胞系的增殖，其 IC50 值分别为 79.51 nM、25.77 nM 和 40.35 nM，同时对非 AML 血液癌细胞系仅表现出微弱活性[1]。
DC551040 (7 天) 可抑制 AML 患者来源细胞的增殖，在 4 个样本中的 IC50 值范围为 0.68 nM 至 4157 nM[1]。
DC551040 (0.5-4 μM；72 小时) 可在 MV-4-11 急性髓系白血病 (AML) 细胞中诱导剂量依赖性凋亡，凋亡率分别为 7.16%、7.78% 和 10.76%[1]。
DC551040 (24 小时) 可诱导 MV-4-11 急性髓系白血病 (AML) 细胞分化，表现为 CD86 表达升高及特征性形态学改变[1]。
DC551040 (0.1-2 μM；1-7 天) 可呈剂量依赖性上调 MV-4-11 急性髓系白血病 (AML) 细胞中的 H3K4me2 水平[1]。
DC551040 对正常外周血单个核细胞毒性较低，其 IC50 大于 10 μM[1]。
DC551040 (1-5 μM；12 小时) 可上调 MV-4-11 急性髓系白血病 (AML) 细胞中 STAT3 的磷酸化水平[1]。
DC551040 (0.3-3 μM；48 小时) 可呈剂量依赖性上调 MOLM-13、MV-4-11 和 HL-60 急性髓系白血病 (AML) 细胞中 IL6、MYC、CCL5 及 VEGFA 的 mRNA 表达[1]。
DC551040 (0.23-5000 nM；10 天) 与 HHT (HY-14944) 可协同抑制 MOLM-13、MV-4-11、HL-60、Kasumi-1 急性髓系白血病 (AML) 细胞系以及 AML 患者来源细胞的增殖，联合处理 10 天后可产生较高的协同评分 (ZIP >10，Bliss score 21.25)[1]。
DC551040 (0.5 μM；24 小时) 联合 HHT 可显著提高经 24 h 处理后的 MV-4-11 急性髓系白血病 (AML) 细胞中 Caspase 3/7 的活性[1]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

DC551040 相关抗体:

Western Blot Analysis[1]

Cell Line: MV-4-11 AML cells
Concentration: 50 nM; 250 nM
Incubation Time: 24 h
Result: Disrupted the association between LSD1 and GFI1B, as shown by reduced co-immunoprecipitation of LSD1 with GFI1B.

Apoptosis Analysis[1]

Cell Line: MV-4-11 AML cells
Concentration: 0.5 μM; 2 μM; 4 μM
Incubation Time: 72 h
Result: Induced apoptosis in a dose-dependent manner: 7.16% apoptosis at 0.5 μM, 7.78% at 2 μM, and 10.76% at 4 μM, compared to 4.07% in the DMSO control.

Western Blot Analysis[1]

Cell Line: MV-4-11 AML cells
Concentration: 0.1 μM; 0.5 μM; 2 μM
Incubation Time: 1 day, 3 days, 5 days, 7 days
Result: Increased H3K4me2 levels in a dose-dependent manner across all time points: at 1 day, relative ratios were 1.01 at 0.1 μM, 1.25 at 0.5 μM, 1.25 at 2 μM; at 3 days, 1.20 at 0.1 μM, 1.67 at 0.5 μM, 1.51 at 2 μM; at 5 days, 1.22 at 0.1 μM, 1.52 at 0.5 μM, 1.53 at 2 μM; at 7 days, 1.11 at 0.1 μM, 1.25 at 0.5 μM, 1.35 at 2 μM.

Western Blot Analysis[1]

Cell Line: MV-4-11 AML cells
Concentration: 1 μM; 5 μM
Incubation Time: 12 h
Result: Upregulated phosphorylation of STAT3.

Real Time qPCR[1]

Cell Line: MOLM-13, MV-4-11, HL-60 AML cells
Concentration: 0.3 μM; 1 μM; 3 μM
Incubation Time: 48 h
Result: Dose-dependently upregulated IL6 mRNA expression in MOLM-13, MV-4-11, and HL-60 cells.
Dose-dependently upregulated MYC, CCL5, and VEGFA mRNA expression in MOLM-13 cells.

Apoptosis Analysis[1]

Cell Line: MV-4-11 AML cells
Concentration: 0.5 μM; 0.5 μM plus 5 nM HHT
Incubation Time: 24 h
Result: Significantly increased Caspase 3/7 activity (to ~3-fold) compared to either monotherapy (both ~1.5-fold) or DMSO control (~1-fold).
药代动力学
(Parmacokinetics)
Species Dose Route AUC0-t MRT0-t CL F Vss Cmax T1/2 Tmax
Mice[1] 20 mg/kg p.o. 2566 ng·h/mL / / 74.4 % 18.6 L/kg 1257 ng/mL 7.96 h 0.5 h
Mice[1] 10 mg/kg i.v. 1712 ng·h/mL 3.18 h 97.4 mL/min/kg / / / / /
Rat[1] 20 mg/kg p.o. 5777 ng·h/mL / / 92.0 % 14.0 L/kg 851 ng/mL 3.34 h 3 h
Rat[1] 10 mg/kg i.v. 3133 ng·h/mL 4.37 h 53.2 mL/min/kg / / / / /
Dog[1] 5 mg/kg p.o. 10940 ng·h/mL / / 78.6 % 6.76 L/kg 850 ng/mL 10.5 h 1.2 h
Dog[1] 2 mg/kg i.v. 10940 ng·h/mL 6258 h 19.5 mL/min/kg / / / / /
体内研究
(In Vivo)

DC551040 (0.5-2 mg/kg；口服；每日；17 天) 在 Kasumi-1 异种移植小鼠中表现出剂量依赖性抗肿瘤活性，在每日 2 mg/kg 口服给药条件下达到 86.99% 的最高 TGI[1]。
DC551040 (5-10 mg/kg；口服；每日一次；连续 22 天) 在 MV-4-11 异种移植小鼠中发挥剂量依赖性抗肿瘤活性，在 10 mg/kg 每日口服给药条件下达到 61.23% 的 TGI，并可诱导分化标志物 CD86 呈剂量依赖性上调[1]。
DC551040 (0.5-4 mg/kg；口服；每日一次；连续 21 天) 可呈剂量依赖性延长播散性 MV-4-11 急性髓系白血病小鼠的生存期[1]。
DC551040 (1 mg/kg；口服；每日一次；连续 28 天) 与 HHT 协同作用，可显著延长播散性 MV-4-11 AML 小鼠的生存期[1]。
DC551040 (2 mg/kg；口服；每日一次；连续 21 天) 可降低 AML 患者来源异种移植小鼠的残留白血病负荷，并与 HHT 协同增强该效应[1]。
DC551040 (2 mg/kg；口服；每日；持续 21 天) 可在 MV-4-11 异种移植瘤中诱导免疫和炎症通路的动态激活，同时引发时间依赖性的代谢重编程[1]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Nu/Nu nude mice (subcutaneously inoculated in the right flank with 5 × 106 Kasumi-1 cells for a subcutaneous xenograft model)[1]
Dosage: 0.5 mg/kg; 1 mg/kg; 2 mg/kg
Administration: p.o.; daily; 17 days
Result: Demonstrated dose-dependent tumor suppressive activity, with corresponding tumor growth inhibition (TGI) rates of 48.82%, 60.81%, and 86.99%, respectively.
Exhibited superior antitumor effect at 2 mg/kg compared to GSK2879552 (HY-18632) at 2 mg/kg.
Animal Model: Nu/Nu nude mice (subcutaneously inoculated in the right flank with 5 × 106 MV-4-11 cells for a subcutaneous xenograft model)[1]
Dosage: 5 mg/kg; 10 mg/kg
Administration: p.o.; daily; 22 days
Result: Demonstrated dose-dependent tumor suppressive activity, with TGI rates of 41.08% and 61.23%, respectively.
Showed significantly better tumor inhibitory effect at 10 mg/kg compared to GSK2879552 at 10 mg/kg .
Caused dose-dependent upregulation of CD86 positivity in tumor tissues, with higher CD86 expression observed at 10 mg/kg compared to 5 mg/kg.
Animal Model: B-NDG mice (received tail
vein injection of 1 × 107 MV-4-11 cells for intravenous engraft-
ment)[1]
Dosage: 0.5 mg/kg; 2 mg/kg; 4 mg/kg
Administration: p.o.; daily; 21 days
Result: Demonstrated dose-dependent improvement in mouse survival, with longer survival observed at higher doses compared to vehicle control.
Animal Model: B-NDG mice (received tail
vein injection of 1 × 107 MV-4-11 cells for intravenous engraft-
ment)[1]
Dosage: 1 mg/kg
Administration: p.o.; daily; 28 days
Result: Combination treatment with homoharringtonine (HHT, 0.5 mg/kg) significantly extended median mouse survival to 57.5 days, compared to 47.5 days for monotherapy and 48.5 days for HHT monotherapy.
Animal Model: B-NDG mice (received tail
vein injection of 1 × 107 primary AML cells for intravenous engraft-
ment)[1]
Dosage: 2 mg/kg
Administration: p.o.; daily; 21 days
Result: Significantly reduced the proportion of human CD33+ cells in mouse bone marrow compared to vehicle control.
Combination treatment with HHT (0.5 mg/kg) produced a further significant reduction in CD33+ cells, demonstrating a synergistic effect.
Animal Model: Nu/Nu nude mice (subcutaneously inoculated in the right flank with 5 × 106 MV-4-11 cells for a subcutaneous xenograft model)[1]
Dosage: 2 mg/kg
Administration: p.o.; daily; up to 21 days
Result: Induced dynamic changes in protein and gene expression: 233, 276, and 256 proteins were significantly changed at 3, 7, and 21 days, respectively (|log2(fold change)| > 0.585 and p < 0.05).
Activated immune and inflammation-related pathways (including IL6-JAK-STAT3, IL2-STAT5, interferon-γ response) across all time points.
Caused time-dependent alterations in metabolic pathways: oxidative phosphorylation was weakened at 21 days, carbon metabolism and glycolysis/gluconeogenesis were enhanced at 21 days, fatty acid metabolism decreased at 3 days then increased at 7 and 21 days.
分子量

389.51

Formula

C22H32FN3O2
CAS 号
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

DC551040 相关分类

  • 摩尔计算器

  • 稀释计算器

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

DC5510402133291-32-2DC 551040DC-551040Histone DemethylaseApoptosisKasumi-1LSD2AMLacute myeloid leukemiaHL-60MV-4-11MAO-Alysine demethylase 1MAO-BLSD1Inhibitorinhibitorinhibit

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