I would recommend that you use your empirical IC50, as there can be many variables that affect phenotypic outcomes in live cell experiments from lab-to-lab and year-to-year. If your IC50 is 100 times different than others, then maybe it would be wise to figure out why, but if it is within a reasonable range, empirical is best. Particularly if it is consistent for you. Make sure that your data are solid, and include them in any reports wherein you have used the IC50.

Dear Omar,

For pancreatic ductal adenocarcinoma cells AsPC-1, BxPC-3, MIA PaCa-2 and Panc-1, gemcitabine IC50 ranged from 494nM to 23.9 μM.

If your value is within this range you should be satisfied.

For more details please read the following publication:

Carcinogenesis. 2013 Oct;34(10):2361-9. doi: 10.1093/carcin/bgt227. Epub 2013 Jun 26.

Comparative benefits of Nab-paclitaxel over gemcitabine or polysorbate-based docetaxel in experimental pancreatic cancer.

Awasthi N1, Zhang C, Schwarz AM, Hinz S, Wang C, Williams NS, Schwarz MA, Schwarz RE.

Author information

Abstract

Gemcitabine has limited clinical benefits in pancreatic ductal adenocarcinoma. The solvent-based traditional taxanes docetaxel and paclitaxel have not shown clinical results superior to gemcitabine. Nab-paclitaxel, a water-soluble albumin-bound paclitaxel, may carry superior distribution properties into the tumor microenvironment and has shown efficacy in multiple tumor types. We evaluated nab-paclitaxel effects compared with gemcitabine or docetaxel. For pancreatic ductal adenocarcinoma cells AsPC-1, BxPC-3, MIA PaCa-2 and Panc-1, gemcitabine IC50 ranged from 494nM to 23.9 μM; docetaxel IC50 range was from 5 to 34nM; nab-paclitaxel IC50 range was from 243nM to 4.9 μM. Addition of IC25 dose of docetaxel or nab-paclitaxel decreased gemcitabine IC50. Net tumor growth inhibition after gemcitabine, docetaxel or nab-paclitaxel was 67, 31 and 72%, which corresponded with intratumoral proliferative and apoptotic indices. Tumor stromal density was decreased by nab-paclitaxel and to a lesser extent by docetaxel as measured through reduction in α-smooth muscle actin, S100A4 and collagen 1 expression. Animal survival was prolonged after nab-paclitaxel treatment (41 days, P < 0.002) compared with gemcitabine (32 days, P = 0.005), docetaxel (32 days, P = 0.005) and controls (20 days). Survival in nab-paclitaxel/gemcitabine and docetaxel/gemcitabine sequential treatment groups was not superior to nab-paclitaxel alone. Low-dose combination of gemcitabine with nab-paclitaxel or docetaxel was more effective compared with controls or gemcitabine alone but not superior to regular dose nab-paclitaxel alone. Combination treatment of gemcitabine+nab-paclitaxel or gemcitabine+docetaxel increased gemcitabine concentration in plasma and tumor. The superior antitumor activity of nab-paclitaxel provides a strong rationale for considering nab-paclitaxel as first-line monotherapy in pancreatic ductal adenocarcinoma.

http://www.ncbi.nlm.nih.gov/pubmed/23803690

Hoping this will be helpful,

Rafik

Dear Omar,

For pancreatic ductal adenocarcinoma cells AsPC-1, BxPC-3, MIA PaCa-2 and Panc-1, gemcitabine IC50 ranged from 494nM to 23.9 μM.

If your value is within this range you should be satisfied.

For more details please read the following publication:

Carcinogenesis. 2013 Oct;34(10):2361-9. doi: 10.1093/carcin/bgt227. Epub 2013 Jun 26.

Comparative benefits of Nab-paclitaxel over gemcitabine or polysorbate-based docetaxel in experimental pancreatic cancer.

Awasthi N1, Zhang C, Schwarz AM, Hinz S, Wang C, Williams NS, Schwarz MA, Schwarz RE.

Author information

Abstract

Gemcitabine has limited clinical benefits in pancreatic ductal adenocarcinoma. The solvent-based traditional taxanes docetaxel and paclitaxel have not shown clinical results superior to gemcitabine. Nab-paclitaxel, a water-soluble albumin-bound paclitaxel, may carry superior distribution properties into the tumor microenvironment and has shown efficacy in multiple tumor types. We evaluated nab-paclitaxel effects compared with gemcitabine or docetaxel. For pancreatic ductal adenocarcinoma cells AsPC-1, BxPC-3, MIA PaCa-2 and Panc-1, gemcitabine IC50 ranged from 494nM to 23.9 μM; docetaxel IC50 range was from 5 to 34nM; nab-paclitaxel IC50 range was from 243nM to 4.9 μM. Addition of IC25 dose of docetaxel or nab-paclitaxel decreased gemcitabine IC50. Net tumor growth inhibition after gemcitabine, docetaxel or nab-paclitaxel was 67, 31 and 72%, which corresponded with intratumoral proliferative and apoptotic indices. Tumor stromal density was decreased by nab-paclitaxel and to a lesser extent by docetaxel as measured through reduction in α-smooth muscle actin, S100A4 and collagen 1 expression. Animal survival was prolonged after nab-paclitaxel treatment (41 days, P < 0.002) compared with gemcitabine (32 days, P = 0.005), docetaxel (32 days, P = 0.005) and controls (20 days). Survival in nab-paclitaxel/gemcitabine and docetaxel/gemcitabine sequential treatment groups was not superior to nab-paclitaxel alone. Low-dose combination of gemcitabine with nab-paclitaxel or docetaxel was more effective compared with controls or gemcitabine alone but not superior to regular dose nab-paclitaxel alone. Combination treatment of gemcitabine+nab-paclitaxel or gemcitabine+docetaxel increased gemcitabine concentration in plasma and tumor. The superior antitumor activity of nab-paclitaxel provides a strong rationale for considering nab-paclitaxel as first-line monotherapy in pancreatic ductal adenocarcinoma.

http://www.ncbi.nlm.nih.gov/pubmed/23803690

Hoping this will be helpful,

Rafik

Thanks a lot,  appreciated

One of the main problems with in vitro drug treatment data is that the cell culture conditions can vary from lab to lab.  For example I remember getting hugely lower IC-50 values to those obtained by collaborators, and it was only when I realised that their control cells reached confluence after 2 days of a 7 day experiment whilst my control cells never reached confluence that the same cell lines and the same drugs give different results in different labs.  I would suggest that you design the experiments to determine the IC-50 to mirror your experiments on drug resistance, i.e. the same cell density and time period.

Good luck!

Hi. I guess this reference mentions a different ic50 value for gemcitabine against panc1 

http://ar.iiarjournals.org/content/31/11/3747.full

It is 300millimolar !.. that was strange for me too. 

From our experience with pancreatic cancer cell lines, IC50s of 5-FU varied quite widely (9.0–1805.1 μM), but the IC50s of GEM were found to be stable (6.1–77.6 nM); therefore, GEM has been accepted as a first-line chemotherapeutic drug for the treatment of pancreatic cancer. In contrast, according to these studies, 5FU could be useful not only to inhibit cell growth by its chemotherapeutic actions but also to reduce TS expression to improve sensitivity to GEM.

IC50 of gemcitabine on Miapaca-2 cell line at 48 hr that i extracted like 12micromole but in few papers mentioned wee different.

1 micromole it is mentioned.

which one is correct how could i confirm. can anyone help me on this please?

Thank you

Who know the IC50 of GEM in CT-26? It is really difficult to search.....

Dear @ Omar, Instead of using Gemcitabine, Can we use another drug against pancreatic cancer.

Sourbh Garg of course, there are plenty of different options both for pancreatic and other cancers.

Gemcitabine, which is a nucleoside analog, is often used to study drug resistance and has a different mechanism of action. For this reason, IC50 values usually vary according to different cell types, different experimental conditions, and different assay types.

You can choose another toxic agent such as paclitaxel, fluorouracil, or proper tyrosine kinase inhibitors depending on the type of experiment you will be doing.

Thanks @ Gulsah