25 +
Basic Cell Lines
13 +
Resistant Pairs
10 +
Tumor Entities
4-6
Weeks Turnaround
Why OncoSelect™?
Precision oncology demands robust preclinical models. Our panel integrates well-characterized tumor cell lines, drug-resistant derivatives, and tumor microenvironment components to bridge the gap between in vitro pharmacology and clinical translation.
Genomically Annotated
Each line is annotated with principal driver mutations drawn from public databases and literature, enabling mechanism-of-action–driven model selection rather than empirical screening.
EGFR · KRAS · BRAF · HER2 · BCR-ABL · FLT3 · PIK3CA · TP53
QC-Controlled
Identity confirmed by STR profiling, mycoplasma-negative by qPCR, and supplied with passage number, cell culture recommendations.
STR · Mycoplasma · CoA included
Multi-Modal Efficacy Platform
The panel is architected to support the full spectrum of preclinical oncology research — from single-agent potency profiling to complex microenvironment interplay.
Dose-Response Matrix Analysis · Immuno-Oncology Assessment · Tumor Microenvironment Studies
Choose the Right Panel for Your Stage
OncoSelect™ Basic — Screen fast. 25 clinically annotated lines for primary cytotoxicity ranking. OncoSelect™ Pro — Go deeper. Resistant pairs plus stromal and vascular components for mechanism and combination studies. Custom — Your rules. Substitute lines, add disease subtypes, or build from scratch — we configure to your asset.
OncoSelect™ Basic — 25 Cell Lines
25 well-characterized cell lines across 10 tumor indications. Each model carries a documented driver alteration that defines a patient-relevant genotype — select by mechanism, not by chance.
| Cell Line | Type | Indication | Driver Alteration | Recommended Use |
| Cell Line | Type | Indication | Driver Alteration | Recommended Use |
| A549 | Lung adenocarcinoma) | KRAS G12S | Baseline KRAS-mutant lung cancer model; broad-spectrum cytotoxicity profiling | |
| PC-9 | Lung adenocarcinoma) | EGFR ex19del | EGFR-TKI sensitivity screening; first/second-generation inhibitor benchmarking | |
| NCI-H1975 | Lung adenocarcinoma) | EGFR L858R/T790M | Acquired TKI resistance modeling; osimertinib efficacy evaluation | |
| MCF-7 | ER+ breast carcinoma | PIK3CA E545K | Endocrine therapy combination; PI3K pathway inhibitor screening | |
| T-47D | ER+ breast carcinoma | PIK3CA H1047R | Hormone-dependent drug screening; CDK4/6 inhibitor combination | |
| HCT116 | Colon carcinoma | KRAS G13D, MSI-H | Mismatch repair-deficient model; cytotoxic agent sensitivity baseline | |
| HT-29 | Colon adenocarcinoma | BRAF V600E | BRAF inhibitor screening; MAPK pathway resistance studies | |
| SW620 | Colon adenocarcinoma | KRAS G12V | Metastatic progression model; lymph node derivative for dissemination studies | |
| HepG2 | Hepatoblastoma | CTNNB1 mut | Hepatic CYP retention; efficacy-hepatotoxicity dual assessment | |
| Huh7 | Hepatocellular carcinoma | TP53 Y220C | Comparative hepatotoxicity profiling; paired with HepG2 for differential analysis | |
| MKN-45 | Gastric carcinoma | MET amplification | c-MET inhibitor positive control; ADC and bispecific antibody validation | |
| PANC-1 | Pancreatic ductal adenocarcinoma | KRAS G12D | EMT-prone invasive model; 3D co-culture with CAFs for stromal interaction | |
| BxPC-3 | Pancreatic ductal adenocarcinoma | KRAS wild-type | KRAS-targeted agent negative control; Trop-2-high chassis for ADC screening | |
| SK-OV-3 | Ovarian serous cystadenocarcinoma | HER2 amplified | HER2-targeted therapy sensitivity; chemotherapy combination baseline | |
| A2780 | High-grade ovarian serous adenocarcinoma | TP53 wild-type | Platinum-sensitive control; ovarian chemotherapy benchmarking | |
| OVCAR8 | High-grade ovarian serous adenocarcinoma | p53 deletion | Multi-drug resistant baseline; TNF-resistant apoptosis studies | |
| K562 | Chronic myeloid leukemia | BCR-ABL t(9;22) | TKI positive control; MHC-I-negative NK cell activity target | |
| RAJI | Burkitt lymphoma | MYC t(8;14) | B-cell-targeted agent validation; CAR-T and ADC benchmarking | |
| Jurkat | T-ALL | PTEN null, NOTCH1 mut | T-cell signaling reporter chassis; immunomodulator screening | |
| A375 | Melanoma | BRAF V600E | Melanoma-targeted drug gold standard; BRAF/MEK inhibitor profiling | |
| SK-MEL-28 | Melanoma | BRAF V600E | BRAF/MEK inhibitor sensitivity; long-term drug pressure resistance modeling | |
| U87-MG | Glioblastoma | PTEN null | GBM standard model; orthotopic oncolytic virus and targeted therapy evaluation | |
| U-251 MG | Astrocytoma | p53 mut, PTEN mut | Radioresistant baseline; radiosensitizer and chemoradiation combination | |
| 786-O | Renal cell carcinoma | VHL loss | HIF2α-dependent RCC model; multi-target TKI (sunitinib, sorafenib) benchmarking |
OncoSelect™ Pro — Parent/Resistant Pairs + Tumor Microenvironment
13 parent/resistant pairs and 12 tumor microenvironment components across 6 indications. Follow your asset from monotherapy response through acquired resistance, stromal crosstalk, and vascular targeting — all within one integrated panel.
| Model | Category | Genotype / Derivation | Application |
| Model | Category | Genotype / Derivation | Application |
| A549/taxol | Taxol-selected; KRAS G12S background | Taxane resistance in KRAS-mutant NSCLC; efflux pump and tubulin mutation profiling | |
| Lung Adeno CAFs | Primary human lung adenocarcinoma CAFs | Stromal remodeling; desmoplasia modeling; anti-fibrotic drug response | |
| Lung SCC CAFs | Primary human lung SCC CAFs | Squamous stromal crosstalk; tumor-stroma co-culture with A549 or H1975 | |
| Lung Adeno TECs | Primary human lung adenocarcinoma TECs | Adenocarcinoma vascular targeting; anti-angiogenesis and permeability studies | |
| Lung SCC TECs | Primary human lung SCC TECs | Squamous vascular targeting; hypoxia-driven angiogenesis modeling | |
| MCF-7/Palbociclib | Palbociclib-selected; PIK3CA E545K background | CDK4/6 inhibitor resistance; RB pathway bypass mechanisms | |
| T47D/Palbociclib | Palbociclib-selected; PIK3CA H1047R background | Cross-resistance with MCF-7/Pal; endocrine-CDK combination strategy | |
| Breast CAFs | Primary human breast cancer CAFs | Stroma-dependent efficacy; anti-fibrotic and matrix-degrading agent screening | |
| Breast TECs | Primary human breast cancer TECs | Anti-angiogenesis; vascular normalization and drug penetration assessment | |
| HCT-15 | KRAS G13D, PIK3CA E545K/D549N, MSI-H | Colorectal baseline for sensitivity and resistance modeling | |
| HCT-15/Taxol | Taxol-selected; KRAS G13D background | Microtubule-targeting agent resistance; tubulin isotype switching | |
| HCT-15/5FU | 5-FU-selected; MSI-H background | Thymidylate synthase-mediated resistance; combination salvage strategies | |
| LoVo | KRAS G13D, MSI-H | Colorectal baseline; comparative pairing with HCT-15 | |
| LoVo/Onvansertib | Onvansertib-selected; KRAS G13D background | PLK1 inhibitor resistance; spindle checkpoint adaptation | |
| SW620/Onvansertib | Onvansertib-selected; KRAS G12V background | Comparative PLK1 resistance with LoVo/Onvansertib; KRAS allele effect | |
| Colorectal CAFs | Primary human colorectal cancer CAFs | Desmoplasia modeling; stromal drug response in MSI-H and MSS contexts | |
| Colon TECs | Primary human colon cancer TECs | Colorectal vascular targeting; VEGF-independent angiogenesis mechanisms | |
| AsPC-1 | KRAS G12D, TP53, SMAD4 | Pancreatic baseline for gemcitabine sensitivity and resistance modeling | |
| AsPC-1/GEM | Gemcitabine-selected; KRAS G12D background | Nucleoside analog resistance; RRM1/ENT1-mediated mechanisms; combination rescue | |
| PANC-1/GEM | Gemcitabine-selected; KRAS G12D background | Comparative gemcitabine resistance with AsPC-1/GEM; stromal co-culture evaluation | |
| Pancreatic CAFs | Primary human pancreatic cancer CAFs | Dense stromal microenvironment; CAF-tumor co-culture with PANC-1 or AsPC-1 | |
| OVCAR-8/ADR | Adriamycin-selected; p53-deleted background | Anthracycline resistance; ABC transporter (MDR1) pump studies | |
| A2780/cis | Cisplatin-selected; TP53 wild-type background | DNA damage response defects; platinum resistance mechanisms | |
| A2780/Taxol | Taxol-selected; TP53 wild-type background | Triple-resistant ovarian model; tubulin and efflux pump co-evolution | |
| Ovarian CAFs | Primary human ovarian cancer CAFs | Primary tumor stromal interaction; peritoneal microenvironment modeling | |
| Metastatic Ovarian CAFs | Primary human metastatic ovarian CAFs | Metastatic microenvironment; dissemination and implantation mechanisms | |
| Ovarian TECs | Primary human ovarian cancer TECs | Peritoneal dissemination vascular targeting; ascites microenvironment modeling | |
| K562/Adr | Adriamycin-selected; BCR-ABL background | ABC transporter-mediated MDR; imatinib combination in resistant CML |
Frequently Asked Questions
How are cell lines authenticated?
Every line undergoes STR profiling at the latest working stock generation. Mycoplasma screening is performed by qPCR before release.
Can I mix lines across tiers or request a subset?
Yes. Both Basic and Pro tiers are configurable — you can substitute lines or add custom models without recreating the full panel. Pricing is adjusted on a per-line basis.
What is the expected assay window and reproducibility?
For CTG-based viability assays, Z' factors are typically > 0.6 at the recommended seeding density. Inter-assay CV is generally < 15% for IC50 values across triplicate plates. Specific assay windows are provided in each line's data sheet.
Do you offer screening as a service (CRO mode)?
Yes. Customers can either receive the cells in-house or commission us to run CTG, IC50, 3D spheroid, or co-culture assays in our laboratories, with raw data, curve fits, and an interpretive report delivered. CRO engagement is available for all three tiers.
Ready to accelerate your oncology program?
Talk to our scientific team about the Tumor Efficacy Panel — Basic, Pro, or Custom — and receive a model-selection recommendation tailored to your asset and indication strategy.
