Gemcitabine

Catalog No.S1714 Batch:S171405

Technical Data

Formula	C₉H₁₁F₂N₃O₄
Molecular Weight	263.2	CAS No.	95058-81-4
Solubility (25°C)*	In vitro	DMSO	53 mg/mL (201.36 mM)
		Water	10 mg/mL (37.99 mM)
		Ethanol	Insoluble
* <1 mg/ml means slightly soluble or insoluble. * 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. * Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

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Biological Activity

Description	Gemcitabine, a nucleic acid synthesis inhibitor, is a very potent and specific deoxycytidine analogue, used as chemotherapy. Gemcitabine induces a potent p53-dependent apoptosis.
In vitro	Gemcitabine results in 50% inhibition of growth in the CCRF-CEM human leukemia cell culture assay with IC50 of 1 ng/ml. Gemcitabine combined with deoxycytidine provides about a 1000-fold decrease in biological activity. ^[1] Gemcitabine combined with C225 results in additive cytotoxic effects that increased with increasing gemcitabine concentrations in human pancreatic carcinoma L3.6pl cells. ^[2] Gemcitabine combined with Cisplatin results in synergistic effect in wild-type A2780 and cisplatin-resistant ADDP cells. ^[3]
In vivo	Gemcitabine combined with C225 results in growth inhibition, tumor regression, and abrogation of metastasis in L3.6pl tumors established in the pancreas of nude mice. Gemcitabine treatment alone reduces median tumor volume from 538 to 152 mm³. Gemcitabine reduces the production of vascular endothelial growth factor and interleukin 8 in gemcitabine-treated tumors. ^[2] Gemcitabine is able to dramatically and specifically reduces the number of myeloid suppressor cells found in the spleens of animals bearing large tumors with no significant reductions in CD4(+) T cells, CD8(+) T cells, NK cells, macrophages, or B cells. ^[4] Gemcitabine combined with curcumin shows significant reductions in volume (P = 0.008 versus control; P = 0.036 versus gemcitabine alone), Ki-67 proliferation index (P = 0.030 versus control), NF-kappaB activation, and expression of NF-kappaB-regulated gene products (cyclin D1, c-myc, Bcl-2, Bcl-xL, cellular inhibitor of apoptosis protein-1, cyclooxygenase-2, matrix metalloproteinase, and vascular endothelial growth factor) compared with tumors from control mice treated with olive oil only. Gemcitabine combined with Curcumin is also highly effective in suppressing angiogenesis as indicated by a decrease in CD31(+) microvessel density. ^[5]

Description

Gemcitabine, a nucleic acid synthesis inhibitor, is a very potent and specific deoxycytidine analogue, used as chemotherapy. Gemcitabine induces a potent p53-dependent apoptosis.

In vitro

Gemcitabine results in 50% inhibition of growth in the CCRF-CEM human leukemia cell culture assay with IC50 of 1 ng/ml. Gemcitabine combined with deoxycytidine provides about a 1000-fold decrease in biological activity. ^[1]

Gemcitabine combined with C225 results in additive cytotoxic effects that increased with increasing gemcitabine concentrations in human pancreatic carcinoma L3.6pl cells. ^[2]

Gemcitabine combined with Cisplatin results in synergistic effect in wild-type A2780 and cisplatin-resistant ADDP cells. ^[3]

In vivo

Gemcitabine combined with C225 results in growth inhibition, tumor regression, and abrogation of metastasis in L3.6pl tumors established in the pancreas of nude mice. Gemcitabine treatment alone reduces median tumor volume from 538 to 152 mm³. Gemcitabine reduces the production of vascular endothelial growth factor and interleukin 8 in gemcitabine-treated tumors. ^[2]

Gemcitabine is able to dramatically and specifically reduces the number of myeloid suppressor cells found in the spleens of animals bearing large tumors with no significant reductions in CD4(+) T cells, CD8(+) T cells, NK cells, macrophages, or B cells. ^[4]

Gemcitabine combined with curcumin shows significant reductions in volume (P = 0.008 versus control; P = 0.036 versus gemcitabine alone), Ki-67 proliferation index (P = 0.030 versus control), NF-kappaB activation, and expression of NF-kappaB-regulated gene products (cyclin D1, c-myc, Bcl-2, Bcl-xL, cellular inhibitor of apoptosis protein-1, cyclooxygenase-2, matrix metalloproteinase, and vascular endothelial growth factor) compared with tumors from control mice treated with olive oil only. Gemcitabine combined with Curcumin is also highly effective in suppressing angiogenesis as indicated by a decrease in CD31(+) microvessel density. ^[5]

Protocol (from reference)

Cell Assay:^{^[6]}	Cell lines PC cells Concentrations 1 μM Incubation Time 72 h Method Cells were treated with different concentrations of gemcitabine.
Animal Study:^{^[6]}	Animal Models Female BALB/c nude mice Dosages 5 mg/kg Administration i.p.

References

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Customer Product Validation

: Data from [Nucleic Acids Res, 2014, 42(10), 6436-47]

: Data independently produced by , , Dr. Helen Sadik of Johns Hopkins University

: Data from [Data independently produced by , , Proc Natl Acad Sci USA, 2015, 112(6): 1839-44]

: Data from [Data independently produced by , , Mol Cancer, 2017, 16(1):22]

Selleck's Gemcitabine has been cited by 271 publications

AMG 193, a Clinical Stage MTA-Cooperative PRMT5 Inhibitor, Drives Antitumor Activity Preclinically and in Patients With MTAP-Deleted Cancers [ Cancer Discov, 2024, 10.1158/2159-8290.CD-24-0887]	PubMed: 39282709
TRIM29 facilitates gemcitabine resistance via MEK/ERK pathway and is modulated by circRPS29/miR-770-5p axis in PDAC [ Drug Resist Updat, 2024, 74:101079]	PubMed: 38518727
The molecular interaction pattern of lenvatinib enables inhibition of wild-type or kinase-mutated FGFR2-driven cholangiocarcinoma [ Nat Commun, 2024, 15(1):1287]	PubMed: 38346946
An oncolytic vaccinia virus encoding hyaluronidase reshapes the extracellular matrix to enhance cancer chemotherapy and immunotherapy [ J Immunother Cancer, 2024, 12(3)e008431]	PubMed: 38458640
YBX1 as a therapeutic target to suppress the LRP1-β-catenin-RRM1 axis and overcome gemcitabine resistance in pancreatic cancer [ Cancer Lett, 2024, 602:217197]	PubMed: 39216548
SIRT7 knockdown promotes gemcitabine sensitivity of pancreatic cancer cell via upregulation of GLUT3 expression [ Cancer Lett, 2024, 598:217109]	PubMed: 39002692
Identification of STAM-binding protein as a target for the treatment of gemcitabine resistance pancreatic cancer in a nutrient-poor microenvironment [ Cell Death Dis, 2024, 15(9):657]	PubMed: 39242557
PQR309, a dual PI3K/mTOR inhibitor, synergizes with gemcitabine by impairing the GSK-3β and STAT3/HSP60 signaling pathways to treat nasopharyngeal carcinoma [ Cell Death Dis, 2024, 15(3):237]	PubMed: 38555280
Synergistic antitumor activity between HER2 antibody-drug conjugate and chemotherapy for treating advanced colorectal cancer [ Cell Death Dis, 2024, 15(3):187]	PubMed: 38443386
Olanzapine suppresses mPFC activity-norepinephrine releasing to alleviate CLOCK-enhanced cancer stemness under chronic stress [ Cell Commun Signal, 2024, 22(1):375]	PubMed: 39054537

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SHIPPING AND STORAGE
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