Gemcitabine HCl

Catalog No.S1149 Synonyms: LY188011

Gemcitabine HCl Chemical Structure

Molecular Weight(MW): 299.66

Gemcitabine HCl is a DNA synthesis inhibitor with IC50 of 50 nM, 40 nM, 18 nM and 12 nM in PANC1, MIAPaCa2, BxPC3 and Capan2 cells, respectively.

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Cited by 24 Publications

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Biological Activity

Description Gemcitabine HCl is a DNA synthesis inhibitor with IC50 of 50 nM, 40 nM, 18 nM and 12 nM in PANC1, MIAPaCa2, BxPC3 and Capan2 cells, respectively.
Features Gemcitabine has been used to treat pancreatic cancer and has demonstrated effective anti-tumor activity.
Targets
DNA synthesis (Capan2 cells) [1] DNA synthesis (BxPC3 cells) [1] DNA synthesis (MIAPaCa2 cells) [1] DNA synthesis (PANC1 cells) [1]
12 nM 18 nM 40 nM 50 nM
In vitro

Gemcitabine induced NF-κB activity in BxPC-3, PANC-1, and MIA PaCa-2 cells and decreased the level of the NF-κB inhibitor IκBα in BxPC-3 and PANC-1 cells. Treatment of BxPC-3 cells with low dose Gemcitabine for 48 hours results in a dose-dependent increase in NF-κB binding. In contrast, NF-κB DNA binding is decreased in BxPC-3 cells treated with the higher Gemcitabine doses for 48 h; however, 24-h treatment with these higher doses increases NF-κB binding in BxPC-3 cells [2]
Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
CCRF-CEM M4WxfWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFTXSGVKSzVyPUKuPUDDuSBzLkigcm0> NXPnR4xqOjJ2MkW4PFU>
CCRF-CEM/dCK−/− MojZS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2HSWGlEPTB;MkSwMlQhyrFiMkmuNEDPxE1? NHfOUGUzOjR{NUi4OS=>
L1210 wt NFThS3JIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4i2[GlEPTB;MT6zJOKyKDBwMzDuUS=> MYCyNlQzPTh6NR?=
L1210 10K NFHCSYNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4rRXWlEPTB;MkKuNkDDuSB|Lkeg{txO NUDWV5IyOjJ2MkW4PFU>
TC-1  MUDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmPYTWM2OD1zND63JOKyKDJwODDuUS=> NHXUfWgzOjR{NUi4OS=>
TC-1-GR Mn\MS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYfpW5BbUUN3ME2zOk44KMLzIEWuNUDPxE1? MYiyNlQzPTh6NR?=
MIA PaCa-2 NGjVN4tIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2H5SGlEPTB;NEmuO{DDuSBzNz63JI5O NF75U2IzOjR{NUi4OS=>
PANC-1 MluxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkGxTWM2OD1-IESwNEDPxE1? M2DkblIzPDJ3OEi1
CCRF-CEM NYG3dVl2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MkSwTWM2OD1{LkmgxtEhOS56IH7N MXKyNlQzPTh6NR?=
CCRF-CEM-AraC-8C MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYXOWJNDUUN3ME25PVgvQCEEsTC5MlQhdk1? NF7TNIIzOjR{NUi4OS=>
CCRF-CEM  NY\EPYVPT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYG3fWNzPzJiaB?= NHznW5dKSzVyPUKuNEDDuSByLk[gcm0> M4LoblIyQDVzOESz

... Click to View More Cell Line Experimental Data
Assay
Methods Test Index PMID
Western blot
p70S6K1 / p-S6 / HIF-1α; 

PubMed: 27765914     


Cells were treated with different doses of gemcitabine (0, 1.5 and 2.5 μM), the expression levels of p70S6K1, p-S6 and HIF-1α were determined by Western blotting. GAPDH is used as an internal control. 

LC3-I / LC3-II; 

PubMed: 27384485     


A, E. The levels of LC3-I and LC3-II detected by Western blotting were quantified by densitometry using Image J software. The ratio of LC3-II to LC3-I was evaluated after treated with gemcitabine (MCF-7: 4 μg/ml; MDA-MB-231: 1 μg/ml) for 0 h (control), 12, 24 and 48 h. B, F. The ratio of LC3-II to actin was assayed after treated with gemcitabine, chloroquine (CQ) (MCF-7: 2.5 μM; MDA-MB-231: 5 μM), and gemcitabine plus CQ (added before gemcitabine treatment for 1 h) for indicated time (MCF-7: 48 h; MDA-MB-231: 24 h).

pS-ERα / ERα / pERK / ERK; 

PubMed: 27384485     


MCF-7 and MDA-MB-231 cells were treated by gemcitabine with different concentrations (MCF-7: 0, 2, 4, 8 μg/ml; MDA-MB-231: 0, 0.5, 1, 2 μg/ml), and the phosphorylation of ERα (ser167), ERK (Thr202/Tyr204) and expression of LC3-I and LC3-II were detected.

caspase-3 / caspase-8 / caspase-9; 

PubMed: 16307741     


H1299 and H1299/GR cells were treated with 100 nM gemcitabine for the indicated time periods, and proteins in whole-cell lysates were analyzed by immunoblotting with anti-caspase-3, caspase-8, and caspase-9 antibodies. The arrowheads represent cleavage proteins. β-actin was used as a loading control.

p-JNK / JNK / p-ATF2 / p-c-Jun; 

PubMed: 16307741     


Time-dependent activation of the JNK signaling pathway by gemcitabine treatment. H1299 and H1299/GR cells were treated with 100 nM gemcitabine for the indicated time periods. Cell lysates were then subjected to western blotting using total JNK and phospho-specific antibodies to JNK, c-Jun, and ATF2. Maximal phosphorylation of those molecules is observed in H1299 cells treated with gemcitabine for 48 h.

27765914 27384485 16307741
Immunofluorescence
BMI1; 

PubMed: 27177084     


Gemcitabine enhanced nuclear accumulation of Bmi1 by immunofluorescence staining. 

27177084
Growth inhibition assay
Cell viability ; 

PubMed: 27765914     


A and B. Pancreatic adenocarcinoma cells Bxpc-3 (A) and Panc-1 (B) were treated with gemcitabine (GEM) for 48 h at different doses. The cell viability was analyzed by CCK-8 assay, and normalized to cells without gemcitabine treatment.

27765914
In vivo Intratumoral NF-κB activity is significantly elevated (1.3- to 1.8-fold) in the Gemcitabine-treated mice compared to the PBS-treated mice, suggesting that Gemcitabine also induces NF-κB activation. [2]

Protocol

Cell Research:[2]
+ Expand
  • Cell lines: BxPC-3, MIA PaCa-2, and PANC-1 cells
  • Concentrations: 0.2 μM
  • Incubation Time: 24 hours or 48 hours
  • Method: BxPC-3, MIA PaCa-2, and PANC-1 cells are seeded in a 96-well plate. After 24 hours, cells are treated with vehicle, DMAPT and/or Gemcitabine for an additional 24 hours or 48 hours. Apoptosis is quantified using the Cell Death Detection ELISA to detect the amount of cytoplasmic histone-associated DNA fragments and expressed relative to vehicle-treated cells.
    (Only for Reference)
Animal Research:[2]
+ Expand
  • Animal Models: Athymic nude mice with MIA PaCa-2 cells
  • Formulation: Phosphate-buffered saline
  • Dosages: 50 mg/kg or 100 mg/kg
  • Administration: Administered via i.p.
    (Only for Reference)

Solubility (25°C)

In vitro Water 19 mg/mL (63.4 mM)
DMSO Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
Saline
For best results, use promptly after mixing. 		19mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 299.66
Formula

C9H11F2N3O4.HCI
CAS No. 122111-03-9
Storage powder
in solvent
Synonyms LY188011

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03417921 Not yet recruiting Pancreatic Cancer Ability Pharmaceuticals SL|The Cleveland Clinic December 1 2019 Phase 1|Phase 2
NCT03417921 Not yet recruiting Pancreatic Cancer Ability Pharmaceuticals SL|The Cleveland Clinic December 1 2019 Phase 1|Phase 2
NCT03865563 Not yet recruiting Pancreatic Adenocarcinoma Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins July 2019 Phase 1
NCT03865563 Not yet recruiting Pancreatic Adenocarcinoma Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins July 2019 Phase 1
NCT03697564 Not yet recruiting Pancreatic Cancer Stage IV Hitendra Patel|Stand Up To Cancer|Bristol-Myers Squibb|University of California San Diego July 2019 Phase 2
NCT03697564 Not yet recruiting Pancreatic Cancer Stage IV Hitendra Patel|Stand Up To Cancer|Bristol-Myers Squibb|University of California San Diego July 2019 Phase 2

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Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

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Frequently Asked Questions

  • Question 1:

    What’s the difference between S1714 and S1149 and which one is better?

  • Answer:

    They have the same biological activities. The free base(S1714) dissolves better in DMSO, and the hydrochloride (S1149) dissolves better in water.

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DNA/RNA Synthesis Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID