2. Metabolic Enzyme/Protease Cell Cycle/DNA Damage Apoptosis
  3. NAMPT DNA/RNA Synthesis Apoptosis
  4. Nampt-IN-18

Nampt-IN-18 (Compound Q24) 是一种口服有效的 NAMPT 抑制剂，对 hNAMPT 的 IC50 为 8.0 nM。Nampt-IN-18 抑制 NAMPT 酶活性。Nampt-IN-18 抑制 DNA 合成 (DNA synthesis) ，诱导凋亡 (Apoptosis)。Nampt-IN-18 对胃癌和结直肠癌具有抗癌活性。Nampt-IN-18 可用于胃肠道癌症的研究。

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Nampt-IN-18

Nampt-IN-18 Chemical Structure

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Nampt-IN-18 相关抗体

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RNASE L DNA Polymerases RNA Polymerases Helicases DNA Ligase

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

Nampt-IN-18 (Compound Q24) is an orally active NAMPT inhibitor with an IC50 of 8.0 nM against hNAMPT. Nampt-IN-18 inhibits NAMPT enzymatic activity. Nampt-IN-18 inhibits DNA synthesis and induces Apoptosis. Nampt-IN-18 exhibits anticancer activity against gastric cancer and colorectal cancer. Nampt-IN-18 can be used for the research of gastrointestinal cancers[1].

IC50 & Target

IC50: 8.0 nM against hNAMPT[1]
体外研究
(In Vitro)

Nampt-IN-18 (30 min) 可强效抑制重组 hNAMPT 酶活性，其 IC50 为 8.0 ± 1.9 nM[1]。
Nampt-IN-18 (72 h) 可强效抑制 HGC-27 胃癌细胞活力，其 IC50 为 0.69 ± 0.14 nM[1]。
Nampt-IN-18 (72 h) 可抑制 LOVO 结肠癌细胞的活力，其 IC50 为 63 ± 12 nM[1]。
Nampt-IN-18 (72 h) 可抑制 Caco-2 结直肠腺癌细胞活力，其 IC50 为 6.5 ± 2.2 nM[1]。
Nampt-IN-18 (0.25-1 nM; 24 h) 可剂量依赖性地抑制 HGC-27 胃癌细胞中的 DNA 合成，在 1 nM 时观察到强烈的抑制作用[1]。
Nampt-IN-18 (1-4 nM; 48 h) 诱导 HGC-27 胃癌细胞出现显著的 G1 期和 G2/M 期细胞周期阻滞[1]。
Nampt-IN-18 (1-4 nM; 48 h) 可剂量依赖性地诱导 HGC-27 胃癌细胞发生凋亡[1]。
Nampt-IN-18 (0.25-1 nM; 24 h) 可呈剂量依赖性抑制 HGC-27 胃癌细胞的迁移[1]。

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

Nampt-IN-18 相关抗体:

Apoptosis Analysis[1]

Cell Line: Human gastric cancer HGC-27 cells
Concentration: 1-4 nM
Incubation Time: 48 h
Result: Induced measurable apoptosis (~5-11% apoptotic cells) at 1-2 nM.
Induced ~53% apoptotic cells at 4 nM.
药代动力学
(Parmacokinetics)
Species Dose Route T1/2 Tmax Cmax MRT0-∞ CL
Rat[1] 10 mg/kg i.g. 1.86 h 0.67 h 67.43 μg/L 2.51 h 68.63 L/h/kg
体内研究
(In Vivo)

Nampt-IN-18 (3.75-15 mg/kg；灌胃；每日两次；连续 12 天) 在 HGC-27 胃癌异种移植模型中展现出强效的体内抗肿瘤活性[1]。
Nampt-IN-18 (300 mg/kg；灌胃；单次剂量) 对健康 KM 小鼠具有良好的耐受性，未观察到急性毒性或器官损伤[1]。

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

Animal Model: BALB/c nude mice[1]
Dosage: 3.75 mg/kg; 7.5 mg/kg; 15 mg/kg
Administration: i.g.; bid; 12 consecutive days
Result: Achieved a tumor growth inhibition (TGI) rate of 68.9% at 15 mg/kg dose.
Caused no significant body weight loss across all tested doses (15 mg/kg caused transient early weight loss with subsequent recovery to levels not significantly different from the vehicle group).
Reduced terminal tumor weights significantly at all tested doses compared to the vehicle group.
Detected no histopathological abnormalities in the heart, liver, spleen, lung, or kidney at any tested dose.
分子量

475.56

Formula

C27H30FN5O2
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

Nampt-IN-18 相关分类

  • 摩尔计算器

  • 稀释计算器

The molarity calculator equation

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

质量   浓度   体积   分子量 *
= × ×

The dilution calculator equation

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

浓度 (start) × 体积 (start) = 浓度 (final) × 体积 (final)
× = ×
C1   V1   C2   V2
Help & FAQs
  • 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:

Nampt-IN-18NAMPTDNA/RNA SynthesisApoptosisNicotinamide phosphoribosyl transferasePBEFVisfatinpre-B cell-enhancing factorPre-B cell colony enhancing factorCaco-2 colorectal adenocarcinoma cellscell cycle arrestHGC-27 gastric cancer cellsxenograft modelsapoptosisGES-1 cellsLOVO colon cancer cellsgastrointestinal cancersenergy metabolismInhibitorinhibitorinhibit

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