2. Apoptosis Metabolic Enzyme/Protease
  3. Apoptosis Glycosidase
  4. Gal-dMor-Gem

Gal-dMor-Gem 是选择性的衰老细胞清除剂、凋亡 (Apoptosis) 诱导剂、Gemcitabine (HY-17026) 前药。Gal-dMor-Gem 在酯酶 (Esterases) 和 β-gal 激活下释放 Gemcitabine。Gal-dMor-Gem 减少 SA-β-gal、优先诱导衰老细胞凋亡、调控凋亡相关蛋白、在衰老组织中富集并改善衰老相关器官表型。Gal-dMor-Gem 可用于化疗诱导的衰老相关研究。

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Gal-dMor-Gem

Gal-dMor-Gem Chemical Structure

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Gal-dMor-Gem 相关抗体

Top Publications Citing Use of Products

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

Gal-dMor-Gem is a selective senescent cell scavenger, Apoptosis inducer, and a prodrug of Gemcitabine (HY-17026). Gal-dMor-Gem releases Gemcitabine upon activation by Esterases and β-gal. Gal-dMor-Gem reduces SA-β-gal, preferentially induces apoptosis in senescent cells, regulates apoptosis-related proteins, accumulates in senescent tissues, and ameliorates senescence-related organ phenotypes. Gal-dMor-Gem is applicable to research on chemotherapy-induced senescence[1].

体外研究
(In Vitro)

Gal-dMor-Gem (0.1-100 μM; 48 h) 可强效且选择性地降低衰老型 A549/Dox 和 A549/H2O2 细胞的存活率，效果优于非衰老型 A549 细胞；其衰老裂解指数分别为 48.3 和 56.7，IC50 值分别为 1.58 μM 和 1.40 μM[1]。
Gal-dMor-Gem (酯酶 100 U/mL，β-半乳糖苷酶 5 U/mL) 在酯酶和 β-gal 激活下释放活性吉西他滨 (Gem) 的速率快于 Gal-Gem 和 Gal-Mor-Gem，3 h 后释放率达 79.9%，12 h 后累积释放率达 92.4%[1]。
Gal-dMor-Gem (3-48 h) 比 Gal-Gem 更快、更有效地清除衰老的 A549/Dox 细胞，处理 36 h 后可将细胞活力降至 20.9%[1]。
Gal-dMor-Gem (100 μM; 36 h) 可选择性诱导衰老 A549/Dox 细胞发生细胞凋亡，而对非衰老 A549 细胞无该选择性[1]。

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

Gal-dMor-Gem 相关抗体:

Cell Viability Assay[1]

Cell Line: nonsenescent A549 cells, senescent A549/Dox cells, senescent A549/H2O2 cells
Concentration: 0.1-100 μM
Incubation Time: 48 h
Result: Showed selective cytotoxicity toward senescent cells over nonsenescent cells.
Reduced cell viability to 91.7% for A549, 83.0% for A549/Dox, and 80.6% for A549/H2O2 at 0.1 μM.
Reduced cell viability to 57.1% for A549, 17.8% for A549/Dox, and 11.3% for A549/H2O2 at 100 μM.
Achieved IC50 values of 79.54 μM for A549, 1.58 μM for A549/Dox, and 1.40 μM for A549/H2O2.
Resulted in senolytic indices of 48.3 (A549/Dox) and 56.7 (A549/H2O2).

Apoptosis Analysis[1]

Cell Line: nonsenescent A549 cells, senescent A549/Dox cells
Concentration: 100 μM
Incubation Time: 36 h
Result: Induced apoptosis in 10.1% of nonsenescent A549 cells and 50.4% of senescent A549/Dox cells.
Induced lower apoptosis in nonsenescent A549 cells and higher apoptosis in senescent A549/Dox cells compared to Gal-Gem, which induced apoptosis in 21.5% of nonsenescent A549 cells and 32.0% of senescent A549/Dox cells.
药代动力学
(Parmacokinetics)
Species Dose Route Cmax Tmax T1/2 MRT0-t AUC0-t AUC0-∞
Mice[1] 1.0 mg/kg i.p. 254 ng/mL 3.47 h 8.49 h 6.50 h 752 ng·h/mL 775 ng·h/mL
体内研究
(In Vivo)

Gal-dMor-Gem (0.2-1.0 mg/kg；腹腔注射；每周 1 次；共 3 剂) 可有效缓解小鼠体内阿霉素 (Dox) 诱导的全身性衰老，其中 1.0 mg/kg 剂量可将大多数衰老相关标志物恢复至接近健康水平[1]。

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

Animal Model: C57BL/6J mice (Dox-induced systemic senescence model)[1]
Dosage: 0.2 mg/kg; 0.5 mg/kg; 1.0 mg/kg
Administration: i.p.; once weekly; 3 doses
Result: Increased body weight in treated senescent mice relative to untreated controls; achieved 14.6% body weight increase at 0.5 mg/kg and 17.8% body weight increase at 1.0 mg/kg relative to day 10.
Improved liver (ALT, AST) and kidney (CREA, UREA) function markers across all doses, with greater restorative effects than the reference compound at 0.5 mg/kg.
Reduced lung SA-β-gal-positive cells from 62.4% to 44.2% at 0.2 mg/kg, to 16.9% at 0.5 mg/kg, and to 9.9% at 1.0 mg/kg (approaching healthy levels of 6.0%).
Increased lung LMNB1-positive nuclei from 43.9% to 57.6% at 0.2 mg/kg, to 74.9% at 0.5 mg/kg, and to 82.0% at 1.0 mg/kg (approaching healthy levels of 86.0%).
Reduced lung relative IL-6 fluorescence intensity from 1450.5 to 1205.0 at 0.2 mg/kg, to 678.1 at 0.5 mg/kg, and to 450.0 at 1.0 mg/kg.
Reduced liver SA-β-gal-positive cells from 88.1% to 63.7% at 0.2 mg/kg, to 21.7% at 0.5 mg/kg, and to 13.2% at 1.0 mg/kg (approaching healthy levels of 6.9%).
Reduced liver relative p21 expression from 0.93 to 0.78 at 0.2 mg/kg, to 0.58 at 0.5 mg/kg, and to 0.50 at 1.0 mg/kg.
Reduced liver relative p53 expression to 0.49 at 0.5 mg/kg and to 0.43 at 1.0 mg/kg (approaching healthy levels of 0.38).
Reduced SA-β-gal-positive cells, increased LMNB1-positive nuclei, and reduced IL-6 levels in heart and kidney across all doses, with greater effects than the reference compound at 0.5 mg/kg; restored these markers to near healthy levels at 1.0 mg/kg.
分子量

939.91

Formula

C42H55F2N5O17
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

Gal-dMor-Gem 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?

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Keywords:

Gal-dMor-GemApoptosisGlycosidasesenescent cellsgemcitabineBeas-2B cellschemotherapy-induced senescencesenescence-associated β-galactosidaseA549 cellsSA-β-galA549/Dox cellsA549/H2O2 cellsMDA-MB-231 cellsInhibitorinhibitorinhibit

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