
Proactive Engagement Professional Expertise Streamlined Processes
Extensive Tumor Cell Line Resources — 300+ CDX Models, 60+ Syngeneic Cell Lines, 260+ Gene-Edited Cell Lines. Fully Compatible with Small Molecules, Antibodies, ADCs, TCEs, and More.
SOP-Driven Operations — From cell culture to data analysis, ensuring consistent inter-batch performance and reliable results.
Multiple Detection Models Available — Including cell killing, apoptosis, cell cycle, colony formation, combination index (CI), and more.
Complete Pharmacological Report Delivered in 2–4 Weeks — From cell thawing to data analysis, the entire process is efficiently executed.
Experienced Team — With over 100+ projects delivered.
Compliant Data for Regulatory Submission — complete traceability of raw data and images, fully supporting China and US dual filing requirements.
Cell Line Engineering
In vitro Pharmacological Evaluation
Custom Cell Line Engineering
Gene editing is a genetic engineering technique that enables precise modifications—including gene knockouts, insertions, and site-specific point mutations—within target genes or their transcriptional products. These modifications are primarily mediated by engineered nucleases, which facilitate targeted sequence deletion, integration, or precision editing of the genome. The CRISPR-Cas9 system enables efficient knockout or overexpression of specific genes, serving as a powerful tool for target gene screening. When integrated with functional assays, it facilitates the identification of critical genes essential for specific biological processes or disease mechanisms.
GPT has developed an optimized CRISPR-Cas9 platform that delivers enhanced editing efficiency with minimal off-target effects. We provide comprehensive gene editing services encompassing gene knockout, knock-in, overexpression, and luciferase reporter integration. Tailored to the distinct characteristics of individual cell types, we employ the most appropriate delivery methodologies, including lipid-based transfection, electroporation, or lentiviral transduction.
CRISPR Gene Edited Cell Lines
Luciferase Modified Cell Lines
Mouse Derived Cell Lines
CDX
In Vitro Drug Efficacy Screening Platform
Description
In vitro drug efficacy evaluation is a crucial step in preclinical research for drug development, especially for large molecule antibodies, Antibody-Drug Conjugates (ADCs), T-Cell Engagers (TCEs), nucleic acid-based drugs, and small molecules. GemPharmatech's in vitro screening platform offers professional and customized drug efficacy evaluation plans for these diverse drug types. Integrated with our in vitro drug efficacy analysis platform, we provide a one-stop, comprehensive preclinical assessment.
Service Offering
Instruments
| Instrument | Applications |
| Countstar Castor X1 | Cell line development (clonality); Transfection efficiency (GFP/RFP); Confluency analysis. |
| Countleader FL 1000 | Cell counting (e.g., Car-T, PBMC). |
| Agilent BioTek Synergy H1 | UV-Vis absorbance;Fluorescence intensity;Luminescence;Fluorescence polarization;Time-resolved fluorescence.6- to 384-well plates. |
| Cytek full-spectrum | FACS: 3 Lasers, up to 38 Channels |
| Thermo Attune NxT | FACS: 4 Lasers, up to 14 Channels |
Immune checkpoint receptors are essential for immune homeostasis and disease. When developing antibody drugs targeting these checkpoints, antibody-antigen binding is key to assessing function. Antibody binding assays measure in vitro binding to target-positive and humanized mouse cells, and compare with positive controls to guide in vivo efficacy studies.

Fig1. Flow cytometry analysis of Pembrolizumab monoclonal antibody (mAb) and PD-1 expression on immune cells under various conditions.
Antibody-dependent cell-mediated cytotoxicity (ADCC) is a critical immune mechanism where antibodies bridge target cells (such as virus-infected or tumor cells) to effector immune cells, primarily natural killer (NK) cells and cytotoxic T cells. In this process, the antibody's Fab fragment binds to specific surface antigens on target cells, while its Fc fragment engages Fc receptors on effector cells, activating their cytotoxic machinery to directly eliminate the target. As a principal antibody-mediated defense mechanism, ADCC is essential for clearing pathogen-infected cells and contributes significantly to the clinical efficacy of therapeutic antibodies. Consequently, assessing ADCC biological activity has become a vital step in antibody drug development, characterization, and quality control.

Figure 2. A. ADCC Schematic Diagram. B.Rituximab ADCC assay.
Complement-dependent cytotoxicity (CDC) is a cell-killing mechanism triggered when specific antibodies bind to target cell surfaces and activate the classical complement pathway, beginning with C1q binding and followed by activation of C2–C9 to form the membrane attack complex (MAC), which lyses the target cell. Complement proteins are a group of approximately 30 heat-sensitive soluble and membrane-associated proteins in blood and body fluids that exhibit enzymatic activity upon activation. Many anticancer antibodies, such as anti-CD20, CD52, and CEA antibodies, can induce CDC effects.

Fig3. A. CDC Schematic Diagram. B. Rituximab CDC assay.
Antibody-dependent cellular phagocytosis (ADCP) is a process in which immune cells engulf target cells in the presence of antibodies. This process is initiated when the Fab end of the antibody binds to a ligand on the target cell's surface, and the Fc end of the antibody binds to FcγR on the phagocyte's surface. This interaction triggers a series of second messenger responses, resulting in the engulfment of the target cell by the phagocyte. The FcγR-mediated engulfment process not only helps fight infections but also plays a crucial role in cancer treatment.

Figure 4. A. ADCP Schematic Diagram. B. Rituximab ADCP assay. Using two different fluorescent dyes to label target cells and macrophages. After the macrophages ingest the target cells, they emit a double-positive signal (located in Stream graph Q2 quadrant).
Excessive activation or suppression of immune cells drives immune diseases. Primary immune cell experiments (e.g., PBMCs, T cells, NK cells) better reflect in vivo antibody activity. These cells can be stimulated via CD3/CD28, IL2, PHA, LPS, SEB, SEA, DC, or mixed lymphocyte response (MLR). Antibody drug effects are evaluated by measuring cytokine release, immune cell proliferation, or surface marker expression—an essential in vitro screening approach for antibody activity.


Figure 5. A. T cell immune checkpoint. B. Pembrolizumab enhanced IL-2 and IFN-γ productions in PBMC stimulated by SEB. C. Pembrolizumab enhanced IL-2 and IFN-γ productions in MLR assay.
Cytokines are bioactive small proteins produced by stimulated immune cells (e.g., monocytes, T cells) and some non-immune cells (e.g., fibroblasts). They regulate cell functions and immune responses through receptor binding, though chronic overproduction of inflammatory cytokines can promote autoimmunity and cancer. Neutralization experiments are used to assess how effectively neutralizing antibodies interfere with specific cytokine activity.

Figure 6. A. Adalimumab neutralized the apoptotic effects of TNFα (50 ng/mL). B. Necrosis induced by TNF-α in L-929 cells is an important model for studying programmed cell necrosis
Bispecific antibodies (BsAbs) contain two distinct antigen-binding sites, enabling simultaneous binding to two targets. Beyond traditional antibody functions, one site can bind a tumor antigen while the other engages an effector cell (e.g., T/NK cell). Compared to conventional antibodies, bispecific T cell engagers (TCEs or BiTEs) offer advantages in tissue permeability, tumor killing efficiency, off-target rates, and clinical application. In vitro evaluation of T/NK cell-mediated tumor killing by BsAbs is a valuable method for assessing their activity during preclinical research.

Figure 7. In vitro efficacy studies of Tarlatamab. A. TCE mechanism of action. B. Binding assay of Tarlatamab in jurkat and PBMC. C. Binding assay of Tarlatamab in SHP-77(DLL3+) and NCI-H446(DLL3-). Tumor cells were co-cultured with human PBMC at E:T ratio of 5:1 and incubated at the indicated concentrations of either Tarlatamab. The supernatant of SHP-77 was evaluated by ELISA for hIFN-γ (D), and the viability of tumor cells was evaluated by FACS (E).
Antibody-drug conjugates (ADCs) are biopharmaceuticals comprising a tumor antigen-specific monoclonal antibody, a potent cytotoxic payload, and a linker. ADCs bind to surface antigens on tumor cells, are internalized, and release the payload inside lysosomes, leading to selective cell killing. Preclinical in vitro efficacy evaluation assesses the biological activity, mechanism of action, and potency of ADC molecules, serving as a critical step that guides subsequent in vivo studies and clinical translation.

Figure 8. In vitro efficacy studies of DS-8201a. A. Binding assay of DS-8201a in different cancer cell lines. B. Internalization was analyzed by flow cytometry after treating SK-BR-3 with DS-8201a labeled with pHrodo dye. C-E. Cells were seeded. DS-8201a was added after cell adhesion. SK-BR-3 cell cycle was evaluated after 48h (C). SK-BR-3 cell apoptosis was evaluated after 72h (D). Viability of NCI-N87 cells was evaluated with CCK-8 after 5 days (E). F-G. Bystander killing effect of DS-8201a. The HER2-positive SK-BR-3 cells and the HER2-negative MDA-MB-468 cells were mixed at an appropriate ratio and cultured. After cell adhesion, the cells were treated with DS-8201a for 4 days, and the population was analyzed by flow cytometry (F). The number of living cells was determined (G).

Figure 9. In vitro efficacy studies of ABBV-399. A. HER2 and c-Met expression profiling in different cancer cell lines. B. Binding assay of ABBV-399 in different cancer cell lines. C. Cells were seeded. ABBV-399 was added after cell adhesion. Viability of cells was evaluated with CTG after 6 days.
We are equipped with automated liquid handling instruments for high-throughput screening (HTS) of small molecule drugs, supporting rapid and accurate in vitro efficacy evaluation

Figure 10. Cytotoxic effects of different drugs on HT29 and HCT116 cells. HT29 and HCT116 were seeded into a 96-well plate. After cell adhesion, each diluted drug was added. Cell viability was evaluated with CTG after incubation.
Cell scratch assay is a widely used method in laboratories for migration assays. The principle behind this method is that when the cells grow and merge into a monolayer, an empty area is intentionally created on this layer, termed a "scratch". Cells at the edge of the scratch will gradually migrate into the void to “heal” or fill the scratch.

Fig11. A549 cell Scratch assay. A549 cells cultured to 90% confluence were subjected to scratch assays using a 200 μL pipette tip. The cells were then cultured for up to 24 hours under serum-starved conditions, and images were captured to evaluate wound healing.
We have established a comprehensive in vitro efficacy evaluation assays for cell therapy products, offering one-stop services that cover major therapeutic modalities, including CAR-T, CAR-NK, and TCR-T. Our capabilities include:
Target cell killing efficiency assessment (e.g., LDH release assay, luciferase reporter gene activity assay,CFSE/CTV based).
Effector cell phenotyping (e.g., FACS-based detection of activation, exhaustion, and memory markers)
Cytokine secretion profiling (e.g., ELISA, HTRF, CBA).
Functional persistence testing under simulated long-term exposure or repeated tumor rechallenge conditions.
We offer in vitro efficacy evaluation services for oligonucleotide therapeutics to assess target gene silencing at both mRNA and protein levels in primary hepatocytes (e.g., derived from humanized mice) and established cell lines.

Figure 12. In vitro application of primary liver cells from humanized mice for screening small nucleic acid candidate delivery.

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