Gemcitabine HCl

For research use only. Not for use in humans.

Catalog No.S1149 Synonyms: LY188011

52 publications

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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Selleck's Gemcitabine HCl has been cited by 52 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.
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 MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGWzbJJKSzVyPUKuPUDDuSBzLkigcm0> MnfuNlI1OjV6OEW=
L1210 wt M2P6Zmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Ml\RTWM2OD1zLkOgxtEhOC5|IH7N NWHud4RXOjJ2MkW4PFU>
L1210 10K M3jXdmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MV3JR|UxRTJ{LkKgxtEhOy55IN88US=> MkXXNlI1OjV6OEW=
TC-1  M3\MdWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUjJR|UxRTF2LkegxtEhOi56IH7N MXiyNlQzPTh6NR?=
TC-1-GR M3P4Tmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmfXTWM2OD1|Nj63JOKyKDVwMTFOwG0> NHjVU5QzOjR{NUi4OS=>
MIA PaCa-2 M{\VU2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVvJR|UxRTR7LkegxtEhOTdwNzDuUS=> NIXFPZMzOjR{NUi4OS=>
PANC-1 NImxWGpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MoHOTWM2OD1-IESwNEDPxE1? MYGyNlQzPTh6NR?=
CCRF-CEM M4Tmdmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3jPVmlEPTB;Mj65JOKyKDFwODDuUS=> MV2yNlQzPTh6NR?=
CCRF-CEM-AraC-8C NFvTbWJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXzMVHY4UUN3ME25PVgvQCEEsTC5MlQhdk1? MV:yNlQzPTh6NR?=
CCRF-CEM  NIXHU3hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1u5XFczKGh? NFvHdGNKSzVyPUKuNEDDuSByLk[gcm0> NVrHTmttOjF6NUG4OFM>

... Click to View More Cell Line Experimental Data

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

PubMed: 27177084     

Gemcitabine enhanced nuclear accumulation of Bmi1 by immunofluorescence staining. 

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.

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]


Cell Research:[2]
- Collapse
  • 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]
- Collapse
  • 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):
For best results, use promptly after mixing.

* 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


CAS No. 122111-03-9
Storage powder
in solvent
Synonyms LY188011
Smiles Cl.NC1=NC(=O)N(C=C1)C2OC(CO)C(O)C2(F)F

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT04051047 Not yet recruiting Drug: Gemcitabine|Procedure: Tumor biopsy and blood draw Glial Tumor of Brain|Diffuse Intrinsic Pontine Glioma|Glioma University of Michigan Rogel Cancer Center|University of Colorado Denver November 30 2019 Early Phase 1
NCT03669601 Not yet recruiting Drug: AZD6738|Drug: Gemcitabine Cancer CCTU- Cancer Theme|AstraZeneca|Cambridge University Hospitals NHS Foundation Trust September 30 2019 Phase 1
NCT04046887 Not yet recruiting Drug: Lonsurf|Drug: Gemcitabine|Drug: Nab-Paclitaxel Pancreatic Cancer|Pancreatic Ductal Adenocarcinoma Patrick Joseph Loehrer Sr.|Indiana University|Taiho Oncology Inc. August 2019 Phase 1
NCT03865563 Not yet recruiting Drug: Retrograde venous infusion of gemcitabine/lipiodol Pancreatic Adenocarcinoma Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins July 2019 Phase 1

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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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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID