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

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.

For research use only. We do not sell to patients.

Gal-dMor-Gem

Gal-dMor-Gem Chemical Structure

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Gal-dMor-Gem Related Antibodies

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Description

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].

In Vitro

Gal-dMor-Gem (0.1-100 μM; 48 h) potently and selectively reduces the viability of senescent A549/Dox and A549/H2O2 cells, with better efficacy than that on non-senescent A549 cells; its senolytic indices are 48.3 and 56.7, with IC50 values of 1.58 μM and 1.40 μM, respectively[1].
Gal-dMor-Gem (esterase 100 U/mL, β-galactosidase 5 U/mL) releases active gemcitabine (Gem) at a faster rate than Gal-Gem and Gal-Mor-Gem upon activation by esterase and β-gal, with a release rate of 79.9% after 3 h and a cumulative release rate of 92.4% after 12 h[1].
Gal-dMor-Gem (3-48 h) eliminates senescent A549/Dox cells faster and more effectively than Gal-Gem, reducing cell viability to 20.9% after 36 h of treatment[1].
Gal-dMor-Gem (100 μM; 36 h) selectively induces apoptosis in senescent A549/Dox cells, but shows no such selectivity toward non-senescent A549 cells[1].

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

Gal-dMor-Gem Related Antibodies

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.
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
In Vivo

Gal-dMor-Gem (0.2-1.0 mg/kg; intraperitoneal injection; once weekly; 3 doses total) effectively alleviates doxorubicin (Dox)-induced systemic senescence in mice, and the 1.0 mg/kg dose restores most senescence-related markers to levels close to those of healthy controls[1].

MedChemExpress (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.
Molecular Weight

939.91

Formula

C42H55F2N5O17
SMILES

O=C(OCC1=CC(CN2CCOCC2)=C(O[C@H]3[C@H](OC(C)=O)[C@@H](OC(C)=O)[C@@H](OC(C)=O)[C@@H](COC(C)=O)C3)C(CN4CCOCC4)=C1)NC5=NC(N(C=C5)[C@@H]6O[C@@H]([C@H](C6(F)F)O)CO)=O
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Purity & Documentation
References
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Gal-dMor-Gem Related Classifications

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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:

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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