Pancreatic ductal adenocarcinoma (PDAC) is defined by frequent KRAS mutations, SMAD4/CDKN2A loss, and a dense stromal niche. Therapy relies on gemcitabine, nab-paclitaxel, and FOLFIRINOX-class regimens, with PARP benefit in BRCA/PALB2-related disease. We provide antibodies and probes around KRAS, SMAD4, p16, CA19-9, plus MAPK/PARP/chemo-backbone tools for stroma–immune–metabolism crosstalk and resistance studies.
Focus areas: KRAS inhibitors & bypass, stroma targeting & delivery, DDR defects & PARP, checkpoints & CAFs
Commonly used for mechanistic studies; follow your lab SOP, compound datasheets, and ethics approvals.
| Compound | Targets / pathways | Experimental notes |
|---|---|---|
| Gemcitabine | DNA synthesis / nucleotide metabolism (dFdCTP incorporation) | Backbone for PDAC models; mind myelosuppression/scheduling. |
| 5-Fluorouracil (5-FU) | Thymidylate synthase (TS) axis | FOLFIRINOX/FOLFOX backbone; DPD pharmacogenetics affects toxicity risk. |
| Irinotecan | Topoisomerase I | SN-38 exposure links to diarrhea; scale doses carefully in animals. |
| Oxaliplatin | DNA crosslinking (platinum) | FOLFIRINOX component; cold-triggered neuropathy often under-modeled in animals. |
| Olaparib | PARP1/2 | Maintenance/sensitivity models in gBRCA/PALB2/HRD contexts. |
| Trametinib | MEK1/2 | MAPK blockade downstream of KRAS; watch RTK/PI3K bypass feedback. |
| Sotorasib | KRAS G12C | G12C subset; pair genotyping with on-target resistance mechanisms. |