Gemcitabine HCl

For research use only.

Catalog No.S1149 Synonyms: LY188011

70 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 70 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 MX\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFez[lBKSzVyPUKuPUDDuSBzLkigcm0> MUKyNlQzPTh6NR?=
CCRF-CEM/dCK−/− MmjFS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGPuSZNKSzVyPUK0NE41KMLzIEK5MlAh|ryP NELCZlEzOjR{NUi4OS=>
L1210 wt M4C4dmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2rw[WlEPTB;MT6zJOKyKDBwMzDuUS=> MXWyNlQzPTh6NR?=
L1210 10K MoHnS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFTv[3hKSzVyPUKyMlIhyrFiMz63JO69VQ>? MkPGNlI1OjV6OEW=
TC-1  M3zEZmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIDRcW5KSzVyPUG0MlchyrFiMj64JI5O Mlj1NlI1OjV6OEW=
TC-1-GR NUG1RlVbT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnPTTWM2OD1|Nj63JOKyKDVwMTFOwG0> NFPqN3MzOjR{NUi4OS=>
MIA PaCa-2 NYPmfXQ5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mnr6TWM2OD12OT63JOKyKDF5Lkegcm0> NWPZTYdxOjJ2MkW4PFU>
PANC-1 MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2TtOGlEPTB;PjC0NFAh|ryP MkThNlI1OjV6OEW=
CCRF-CEM MkfmS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFz0XmhKSzVyPUKuPUDDuSBzLkigcm0> MorsNlI1OjV6OEW=
CCRF-CEM-AraC-8C NEnGe25Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYTJR|UxRTl7OD64JOKyKDlwNDDuUS=> NF\S[oIzOjR{NUi4OS=>
CCRF-CEM  MVHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGXFTIE4OiCq MXjJR|UxRTJwMDFCtUAxNjZibl2= NESzRXUzOTh3MUi0Ny=>

... 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]
- 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
  • 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
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
NCT04383119 Not yet recruiting Drug: Trabectedin|Drug: Gemcitabine Leiomyosarcoma of Ovary|Soft Tissue Sarcoma Italian Sarcoma Group|PharmaMar September 1 2020 Phase 2
NCT04338763 Not yet recruiting Drug: RP72|Drug: Gemcitabine Pancreatic Cancer|Pancreatic Cancer Non-resectable|Pancreatic Cancer Metastatic Rise Biopharmaceuticals Inc.|Amarex Clinical Research April 30 2020 Phase 1
NCT04241276 Not yet recruiting Drug: ATRA|Drug: Gemcitabine|Drug: nab-paclitaxel Pancreatic Cancer Queen Mary University of London|Medical Research Council|Celgene April 30 2020 Phase 2
NCT03773302 Recruiting Drug: BGJ398|Drug: Gemcitabine|Drug: Cisplatin Advanced Cholangiocarcinoma|FGFR2 Gene Mutation QED Therapeutics Inc. December 27 2019 Phase 3
NCT04131192 Recruiting Drug: Z650|Drug: Gemcitabine Pancreatic Cancer Sunshine Lake Pharma Co. Ltd. November 11 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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DNA/RNA Synthesis Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID