Size | Price | Stock | Qty |
---|---|---|---|
250mg |
|
||
500mg |
|
||
1g |
|
||
2g |
|
||
5g |
|
||
10g |
|
||
Other Sizes |
|
Purity: ≥98%
Gemcitabine (formerly LY-188011, NSC-613327; LY188011, NSC613327; dFdC; dFdCyd; trade name: Gemzar), an approved antimetabolite anticancer drug, is a potent DNA synthesis inhibitor with potential antineoplastic activity. With IC50s of 50 nM, 40 nM, 18 nM, and 12 nM, respectively, it suppresses the growth of PANC1, MIAPaCa2, BxPC3, and Capan2 cells. Difluorodeoxycytidine di- and triphosphate (dFdCDP, dFdCTP) are the active metabolites of gemcitabine that are produced intracellularly. The deoxynucleotide pool available for DNA synthesis is reduced when dFdCDP inhibits ribonucleotide reductase.
Targets |
DNA synthesis
|
|
---|---|---|
ln Vitro |
|
|
ln Vivo |
|
|
Cell Assay |
Proliferation assay. [5]
The effect of curcumin on cell proliferation was determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) uptake method as described previously. The cells (2,000 per well) were incubated with curcumin in triplicate in a 96-well plate and then incubated for 2, 4, or 6 days at 37°C. A MTT solution was added to each well and incubated for 2 h at 37°C. An extraction buffer (20% SDS and 50% dimethylformamide) was added, and the cells were incubated overnight at 37°C. The absorbance of the cell suspension was measured at 570 nm using an MRX Revelation 96-well multiscanner. This experiment was repeated twice, and the statistical analysis (simple linear regression analysis initially and then unpaired Student's t test that revealed significant differences between two sample means) was done to obtain the final values.[5] Apoptosis assay. [5] To determine whether curcumin can potentiate the apoptotic effects of gemcitabine in pancreatic cancer cells, we used a Live/Dead assay kit, which determines intracellular esterase activity and plasma membrane integrity. This assay uses calcein, a polyanionic, green fluorescent dye that is retained within live cells, and a red fluorescent ethidium bromide homodimer dye that can enter cells through damaged membranes and bind to nucleic acids but is excluded by the intact plasma membranes of live cells. Briefly, cells (5,000 per well) were incubated in chamber slides, pretreated with curcumin for 4 h, and treated with gemcitabine for 24 h. Cells were then stained with the assay reagents for 30 min at room temperature. Cell viability was determined under a fluorescence microscope by counting live (green) and dead (red) cells. This experiment was repeated twice and the statistical analysis was done. The values were initially subjected to one-way ANOVA, which revealed significant differences between groups, and then later compared among groups using unpaired Student's t test, which revealed significant differences between two sample means.[5] In a 96-well plate, BxPC-3, MIA PaCa-2, and PANC-1 cells are seeded. Cells are treated for a further 24 or 48 hours with vehicle, DMAPT, and/or Gemcitabine after 24 hours. Using the Cell Death Detection ELISA, apoptosis is measured in relation to vehicle-treated cells by counting the quantity of cytoplasmic histone-associated DNA fragments. |
|
Animal Protocol |
Female BALB/c nude mice
5 mg/kg i.p. After 1 week of implantation, mice were randomized into the following treatment groups (n = 6) based on the bioluminescence measured after the first IVIS imaging: (a) untreated control (olive oil, 100 μL daily); (b) curcumin alone (1 g/kg), once daily p.o.; (c) gemcitabine alone (25 mg/kg), twice weekly by i.p. injection; and (d) combination of curcumin (1 g/kg), once daily p.o., and gemcitabine (25 mg/kg), twice weekly by i.p. injection. Tumor volumes were monitored weekly by the bioluminescence IVIS Imaging System 200 using a cryogenically cooled imaging system coupled to a data acquisition computer running Living Image software. Before imaging, animals were anesthetized in an acrylic chamber with 2.5% isoflurane/air mixture and injected i.p. with 40 mg/mL d-luciferin potassium salt in PBS at a dose of 150 mg/kg body weight. After 10 min of incubation with luciferin, mice were placed in a right lateral decubitus position and a digital grayscale animal image was acquired followed by acquisition and overlay of a pseudocolor image representing the spatial distribution of detected photons emerging from active luciferase within the animal. Signal intensity was quantified as the sum of all detected photons within the region of interest per second. Mice were imaged on days 0, 7, 14, 21, 24, and 31 of treatment. Therapy was continued for 4 weeks and animals were sacrificed 1 week later. Primary tumors in the pancreas were excised and the final tumor volume was measured as V = 2 / 3πr3, where r is the mean of the three dimensions (length, width, and depth). The final tumor volumes were initially subjected to one-way ANOVA and then later compared among groups using unpaired Student's t test. Half of the tumor tissue was formalin fixed and paraffin embedded for immunohistochemistry and routine H&E staining. The other half was snap frozen in liquid nitrogen and stored at −80°C. H&E staining confirmed the presence of tumor(s) in each pancreas.[5] |
|
References | ||
Additional Infomation |
Gemcitabine is a 2'-deoxycytidine having geminal fluoro substituents in the 2'-position. An inhibitor of ribonucleotide reductase, gemcitabine is used in the treatment of various carcinomas, particularly non-small cell lung cancer, pancreatic cancer, bladder cancer and breast cancer. It has a role as a photosensitizing agent, a DNA synthesis inhibitor, a prodrug, an EC 1.17.4.1 (ribonucleoside-diphosphate reductase) inhibitor, an environmental contaminant, a xenobiotic, a radiosensitizing agent, an antineoplastic agent, an antimetabolite, an antiviral drug and an immunosuppressive agent. It is an organofluorine compound and a pyrimidine 2'-deoxyribonucleoside.
ChEBI
Gemcitabine is a nucleoside analog and a chemotherapeutic agent. It was originally investigated for its antiviral effects, but it is now used as an anticancer therapy for various cancers. Gemcitabine is a cytidine analog with two fluorine atoms replacing the hydroxyl on the ribose. As a prodrug, gemcitabine is transformed into its active metabolites that work by replacing the building blocks of nucleic acids during DNA elongation, arresting tumour growth and promoting apoptosis of malignant cells. The structure, metabolism, and mechanism of action of gemcitabine are similar to [cytarabine], but gemcitabine has a wider spectrum of antitumour activity. Gemcitabine is marketed as Gemzar and it is available as intravenous injection. It is approved by the FDA to treat advanced ovarian cancer in combination with [carboplatin], metastatic breast cancer in combination with [paclitaxel], non-small cell lung cancer in combination with [cisplatin], and pancreatic cancer as monotherapy. It is also being investigated in other cancer and tumour types. DrugBank View MoreGemcitabine is a cytosine analogue and intravenously administered antineoplastic agent used in the therapy of several forms of advanced, pancreatic, lung, breast, ovarian and bladder cancer. Gemcitabine is associated with a high rate of transient serum enzyme elevations during therapy but is a very rare cause of acute, clinically apparent liver injury. LiverTox Gemcitabine is a natural product found in Aspergillus violaceofuscus and Penicillium brocae with data available. LOTUS - the natural products occurrence database Gemcitabine is a broad-spectrum antimetabolite and deoxycytidine analogue with antineoplastic activity. Upon administration, gemcitabine is converted into the active metabolites difluorodeoxycytidine diphosphate (dFdCDP) and difluorodeoxycytidine triphosphate (dFdCTP) by deoxycytidine kinase. dFdCTP competes with deoxycytidine triphosphate (dCTP) and is incorporated into DNA. This locks DNA polymerase thereby resulting in "masked termination" during DNA replication. On the other hand, dFdCDP inhibits ribonucleotide reductase, thereby decreasing the deoxynucleotide pool available for DNA synthesis. The reduction in the intracellular concentration of dCTP potentiates the incorporation of dFdCTP into DNA. NCI Thesaurus (NCIt) A deoxycytidine antimetabolite used as an antineoplastic agent. Gemcitabine is a chemotherapeutic agent used as monotherapy or in combination with other anticancer agents. In combination with [carboplatin], it is indicated for the treatment of advanced ovarian cancer that has relapsed at least 6 months after completion of platinum-based therapy. Gemcitabine in combination with [paclitaxel] is indicated for the first-line treatment of patients with metastatic breast cancer after failure of prior anthracycline-containing adjuvant chemotherapy, unless anthracyclines were clinically contraindicated. In combination with [cisplatin], gemcitabine is indicated for the first-line treatment of patients with inoperable, locally advanced (Stage IIIA or IIIB) or metastatic (Stage IV) non-small cell lung cancer (NSCLC). Dual therapy with cisplatin is also used to treat patients with Stage IV (locally advanced or metastatic) transitional cell carcinoma (TCC) of the bladder. Gemcitabine is indicated as first-line treatment for patients with locally advanced (nonresectable Stage II or Stage III) or metastatic (Stage IV) adenocarcinoma of the pancreas. Gemcitabine is indicated for patients previously treated with [fluorouracil]. Gemcitabine is a cytosine analogue and intravenously administered antineoplastic agent used in the therapy of several forms of advanced, pancreatic, lung, breast, ovarian and bladder cancer. Gemcitabine is associated with a high rate of transient serum enzyme elevations during therapy but is a very rare cause of acute, clinically apparent liver injury. Gemcitabine is a nucleoside analog that mediates its antitumour effects by promoting apoptosis of malignant cells undergoing DNA synthesis. More specifically, it blocks the progression of cells through the G1/S-phase boundary. Gemcitabine demonstrated cytotoxic effects against a broad range of cancer cell lines _in vitro_. It displayed schedule-dependent antitumour activity in various animal models and xenografts from human non-small cell lung cancer (NSCLC) and pancreatic cancer. Therefore, the antineoplastic effects of gemcitabine are enhanced through prolonged infusion time rather than higher dosage. Gemcitabine inhibited the growth of human xenografts from carcinoma of the lung, pancreas, ovaries, head and neck, and breast. In mice, gemcitabine inhibited the growth of human tumour xenografts from the breast, colon, lung or pancreas by 69 to 99%. In clinical trials of advanced NSCLC, gemcitabine monotherapy produced objective response rates ranging from 18 to 26%, with a median duration of response ranging from 3.3 to 12.7 months. Overall median survival time was 6.2 to 12.3 months. The combined use of cisplatin and gemcitabine produced better objective response rates compared to monotherapy. In patients with advanced pancreatic cancer, objective response rates in patients ranged from 5.to 12%, with a median survival duration of 3.9 to 6.3 months. In Phase II trials involving patients with metastatic breast cancer, treatment with gemcitabine alone or with adjuvant chemotherapies resulted in response rate ranging from 13 to 42% and median survival duration ranging from 11.5 to 17.8 months. In metastatic bladder cancer, gemcitabine has a response rate 20 to 28%. In Phase II trials of advanced ovarian cancer, patients treated with gemcitabine had response rate of 57.1%, with progression free survival of 13.4 months and median survival of 24 months. Gemcitabine causes dose-limiting myelosuppression, such as anemia, leukopenia, neutropenia, and thrombocytopenia; however, events leading to discontinuation tend to occur less than 1% of the patients. Gemcitabine can elevate ALT, AST and alkaline phosphatase levels. Absorption: Peak plasma concentrations of gemcitabine range from 10 to 40 mg/L following a 30-minute intravenous infusion, and are reached at 15 to 30 minutes. One study showed that steady-state concentrations of gemcitabine showed a linear relationship to dose over the dose range 53 to 1000 mg/m2. Gemcitabine triphosphate, the active metabolite of gemcitabine, can accumulate in circulating peripheral blood mononuclear cells. In one study, the Cmax of gemcitabine triphosphate in peripheral blood mononuclear cells occurred within 30 minutes of the end of the infusion period and increased increased proportionally with gemcitabine doses of up to 350 mg/m2. Route of Elimination: Gemcitabine mainly undergoes renal excretion. Within a week following administration of a single dose of 1000 mg/m2 infused over 30 minutes, about 92-98% of the dose was recovered in urine where 89% of the recovered dose was excreted as difluorodeoxyuridine (dFdU) and less than 10% as gemcitabine. Monophosphate, diphosphate, or triphosphate metabolites of gemcitabine are not detectable in urine. In a single-dose study, about 1% of the administered dose was recovered in the feces. Volume of Distribution: In patients with various solid tumours, the volume of distribution increased with infusion length. The volume of distribution of gemcitabine was 50 L/m2 following infusions lasting less than 70 minutes. For long infusions, the volume of distribution rose to 370 L/m2. Gemcitabine triphosphate, the active metabolite of gemcitabine, accumulates and retains in solid tumour cells _in vitro_ and _in vivo_. It is not extensively distributed to tissues after short infusions that last less than 70 minutes. It is not known whether gemcitabine crosses the blood-brain barrier, but gemcitabine is widely distributed into tissues, including ascitic fluid. In rats, placental and lacteal transfer occurred rapidly at five to 15 minutes following drug administration. Clearance: Following intravenous infusions lasting less than 70 minutes, clearance ranged from 41 to 92 L/h/m2 in males and ranged from 31 to 69 L/h/m2 in females. Clearance decreases with age. Females have about 30% lower clearance than male patients. Metabolism / Metabolites: Following administration and uptake into cancer cells, gemcitabine is initially phosphorylated by deoxycytidine kinase (dCK), and to a lower extent, the extra-mitochondrial thymidine kinase 2 to form gemcitabine monophosphate (dFdCMP). dFdCMP is subsequently phosphorylated by nucleoside kinases to form active metabolites, gemcitabine diphosphate (dFdCDP) and gemcitabine triphosphate (dFdCTP). Gemcitabine is also deaminated intracellularly and extracellularly by cytidine deaminase to its inactive metabolite 2′,2′-difluorodeoxyuridine or 2´-deoxy-2´,2´-difluorouridine (dFdU). Deamination occurs in the blood, liver, kidneys, and other tissues, and this metabolic pathway accounts for most of drug clearance. Biological Half-Life: Following intravenous infusions lasting less than 70 minutes, the terminal half-life ranged from 0.7 to 1.6 hours. Following infusions ranging from 70 to 285 minutes, the terminal half-life ranged from 4.1 to 10.6 hours. Females tend to have longer half-lives than male patients. Gemcitabine triphosphate, the active metabolite of gemcitabine, can accumulate in circulating peripheral blood mononuclear cells. The terminal half-life of gemcitabine triphosphate, the active metabolite, from mononuclear cells ranges from 1.7 to 19.4 hours. Mechanism of Action: Gemcitabine is a potent and specific deoxycytidine analog. After uptake into malignant cells, gemcitabine is phosphorylated by deoxycytidine kinase to form gemcitabine monophosphate, which is then converted to the active compounds, gemcitabine diphosphate (dFdCDP) and gemcitabine triphosphate (dFdCTP). These active metabolites are nucleosides that mediate antitumour effects. dFdCTP competes with deoxycytidine triphosphate (dCTP) for incorporation into DNA, thereby competitively inhibiting DNA chain elongation. The non-terminal position of dFdCTP in the DNA chain prevents detection of dFdCTP in the chain and repair by proof-reading 3′5′-exonuclease: this process is referred to as "masked DNA chain termination." Incorporation of dFdCTP into the DNA chain ultimately leads to chain termination, DNA fragmentation, and apoptotic cell death of malignant cells. Gemcitabine has self-potentiating pharmacological actions that can increase the probability of successful incorporation of gemcitabine triphosphate into the DNA chain: dFdCDP inhibits ribonucleotide reductase, an enzyme responsible for catalyzing the reactions that generate dCTP for DNA synthesis. Since dFdCDP reduces the levels of dCTP, there is less competition for gemcitabine triphosphate for incorporation into DNA. Gemcitabine can also reduce metabolism and elimination of active metabolites from the target ce1l, prolonging high intracellular concentrations of the active metabolites. Such self-potentiating effects are not present with [cytarabine]. Gemcitabine hydrochloride, a synthetic pyrimidine nucleoside, is an antineoplastic agent. The nucleoside analog consists of the pyrimidine base difluorocytidine, and the sugar moiety deoxyribose. Like most antimetabolite antineoplastic agents, gemcitabine is cell-cycle specific, acting principally in the S phase of the cell cycle; the drug also may cause cellular arrest at the G1-S border. The cytotoxic activity of gemcitabine (2'-deoxy-2',2'-difluorocytidine) depends on intracellular conversion to its 5'-diphosphate and -triphosphate metabolites; thus, deoxydifluorocytidine-5?-diphosphate (dFdCDP, gemcitabine diphosphate) and -triphosphate (dFdCTP, gemcitabine triphosphate) and not unchanged gemcitabine are the pharmacologically active forms of the drug. Gemcitabine is phosphorylated by deoxycytidine kinase to gemcitabine monophosphate, which subsequently is phosphorylated to the corresponding diphosphate and triphosphate nucleosides, presumably by deoxycytidylate kinase and nucleoside diphosphate kinase, respectively. The cytotoxic effect of gemcitabine is attributed to the combined actions of its diphosphate and triphosphate nucleosides, which lead to inhibition of DNA synthesis. Gemcitabine diphosphate inhibits ribonucleotide reductase, which is responsible for catalyzing the formation of deoxynucleoside triphosphates needed in DNA synthesis. By inhibiting this reductase, gemcitabine diphosphate interferes with subsequent de novo nucleotide production. Gemcitabine triphosphate inhibits DNA synthesis by competing with the physiologic substrate, deoxycytidine triphosphate, for DNA polymerase and incorporation into DNA. The reduction in intracellular concentrations of deoxycytidine triphosphate induced by gemcitabine diphosphate actually enhances the incorporation of gemcitabine triphosphate into DNA, a mechanism referred to as ''self-potentiation.'' Following incorporation of gemcitabine triphosphate into the DNA chain, a single additional nucleotide, a normal base pair, is added and DNA synthesis is terminated, resulting in apoptosis (programmed cell death). DNA polymerase ? is unable to recognize the abnormal (gemcitabine) nucleotide and repair the DNA strand as a result of masking by the terminal normal base pair nucleotide (masked chain termination). This inability to recognize and excise the abnormal nucleotide results in a prolonged intracellular half-life of gemcitabine compared with other nucleoside analogs such as cytarabine and is thought to contribute to gemcitabine's expanded spectrum of antineoplastic activity relative to such agents. In CEM T lymphoblastoid cells, gemcitabine induces internucleosomal DNA fragmentation, which is characteristic of programmed cell death. |
Molecular Formula |
C9H11F2N3O4
|
|
---|---|---|
Molecular Weight |
263.2
|
|
Exact Mass |
263.07
|
|
Elemental Analysis |
C, 41.07; H, 4.21; F, 14.44; N, 15.97; O, 24.31
|
|
CAS # |
95058-81-4
|
|
Related CAS # |
|
|
PubChem CID |
60750
|
|
Appearance |
White to off-white solid powder
|
|
Density |
1.8±0.1 g/cm3
|
|
Boiling Point |
468.0±55.0 °C at 760 mmHg
|
|
Melting Point |
168.64°C
|
|
Flash Point |
236.8±31.5 °C
|
|
Vapour Pressure |
0.0±2.6 mmHg at 25°C
|
|
Index of Refraction |
1.652
|
|
LogP |
-1.24
|
|
tPSA |
110.60
|
|
SMILES |
C1=CN(C(=O)N=C1N)[C@H]2C([C@@H]([C@H](O2)CO)O)(F)F
|
|
InChi Key |
SDUQYLNIPVEERB-QPPQHZFASA-N
|
|
InChi Code |
InChI=1S/C9H11F2N3O4/c10-9(11)6(16)4(3-15)18-7(9)14-2-1-5(12)13-8(14)17/h1-2,4,6-7,15-16H,3H2,(H2,12,13,17)/t4-,6-,7-/m1/s1
|
|
Chemical Name |
4-amino-1-[(2R,4R,5R)-3,3-difluoro-4-hydroxy-5-(hydroxymethyl)oxolan-2-yl]pyrimidin-2-one
|
|
Synonyms |
|
|
HS Tariff Code |
2934.99.9001
|
|
Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: This product requires protection from light (avoid light exposure) during transportation and storage. |
|
Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
|
Solubility (In Vitro) |
|
|||
---|---|---|---|---|
Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.62 mg/mL (9.95 mM) (saturation unknown) in 5% DMSO + 40% PEG300 + 5% Tween80 + 50% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.62 mg/mL (9.95 mM) (saturation unknown) in 5% DMSO + 95% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. Preparation of 20% SBE-β-CD in Saline (4°C,1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.58 mg/mL (9.80 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. Solubility in Formulation 4: ≥ 2.08 mg/mL (7.90 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL of PEG300 and mix evenly; then add 50 μL of Tween-80 to the above solution and mix evenly; then add 450 μL of normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 5: ≥ 2.08 mg/mL (7.90 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C,1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. Solubility in Formulation 6: ≥ 2.08 mg/mL (7.90 mM) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly. Solubility in Formulation 7: ≥ 2.62 mg/mL (9.95 mM) (saturation unknown) in 5% DMSO + 40% PEG300 + 5% Tween80 + 50% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 8: 20 mg/mL (75.99 mM) in 0.5%HPMC + 1%Tween80 (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication. |
Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
1 mM | 3.7994 mL | 18.9970 mL | 37.9939 mL | |
5 mM | 0.7599 mL | 3.7994 mL | 7.5988 mL | |
10 mM | 0.3799 mL | 1.8997 mL | 3.7994 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration: mg/mL;
Method for preparing DMSO stock solution: mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation::Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
NCT Number | Recruitment | interventions | Conditions | Sponsor/Collaborators | Start Date | Phases |
NCT03507491 | Active Recruiting |
Drug: Gemcitabine Drug: Nab-paclitaxel |
Cancer | Emory University | August 27, 2018 | Phase 1 |
NCT05093322 | Active Recruiting |
Drug: Surufatinib in combination with Gemcitabine |
Solid Tumor Lymphoma |
Hutchmed | November 30, 2021 | Phase 1 Phase 2 |
NCT04634539 | Active Recruiting |
Drug: Gemcitabine Drug: Nab-paclitaxel |
Pancreatic Ductal Adenocarcinoma Pancreatic Cancer |
Jun Gong, MD | May 13, 2021 | Phase 1 |
NCT03520790 | Active Recruiting |
Drug: Gemcitabine Drug: Nab-paclitaxel |
Pancreatic Cancer | Dana-Farber Cancer Institute | December 5, 2018 | Phase 1 Phase 2 |
NCT00479128 | Active Recruiting |
Drug: Bortezomib Drug: Gemcitabine |
Solid Tumor Urethral Cancer |
M.D. Anderson Cancer Center | September 28, 2006 | Phase 1 |