NCI-H1755 Xenograft Model Service for NSCLC

The NCI-H1755 xenograft model provides a robust preclinical platform for investigating BRAF Class II-mutant non-small cell lung cancer (NSCLC), enabling researchers to evaluate tumor growth dynamics, MAPK pathway-targeted therapeutic efficacy, and rational combination strategies in an immunodeficient host. Alfa Cytology delivers comprehensive NCI-H1755 xenograft model services encompassing authenticated cell banking, tumor establishment, compound administration, and multi-layered endpoint analysis to generate reproducible, publication-quality data that advance your preclinical oncology pipeline.

Overview of NCI-H1755 Xenograft Model for NSCLC

The NCI-H1755 cell line was established in October 1987 from a liver metastasis of a patient with Stage 4 lung adenocarcinoma and is classified as a well-differentiated pulmonary adenocarcinoma with mixed epithelial and rounded morphology. Genetically, this line harbors a BRAF G469A mutation—a Class II BRAF alteration characterized by elevated kinase activity and RAS-independent signaling—that accounts for a notable subset of BRAF-mutant NSCLC cases distinct from the more common V600E variant. This molecular profile renders NCI-H1755 particularly valuable for preclinical evaluation of pan-RAF inhibitors, MEK inhibitors, and combination regimens targeting the MAPK cascade in non-V600E BRAF-driven lung cancer.

Fig 1. In the NCI-H1755 (BRAF G469A) xenograft model, exarafenib plus binimetinib significantly suppressed tumor growth versus vehicle and either monotherapy, with sustained p-ERK inhibition in H1755 tumors at 7 h post-dosing. (Manabe, Tadashi, et al., 2026)

In immunodeficient murine hosts, NCI-H1755 cells form reproducible subcutaneous tumors with consistent take rates and moderate growth kinetics, supporting longitudinal tumor volume assessment and pharmacodynamic sampling. The xenograft model has demonstrated significant tumor growth inhibition upon treatment with MEK inhibitor monotherapy and enhanced efficacy with pan-RAF and MEK inhibitor combinations, correlating with suppression of phosphorylated ERK1/2 and downstream effectors such as DUSP6 and EphA2 in tumor lysates. Endpoint tissues are suitable for immunohistochemistry, Western blotting, RNA sequencing, and flow cytometric analysis, providing mechanistic insights into drug response and resistance pathways. These attributes position the NCI-H1755 xenograft as a critical tool for advancing BRAF-directed therapeutic strategies in NSCLC.

Cell Line Information: NCI-H1755

NCI-H1755 is a human lung adenocarcinoma cell line established from a hepatic metastasis, exhibiting mixed adherent and suspension growth characteristics with epithelial-like and rounded morphology. The line carries a BRAF G469A Class II mutation, making it a relevant model for investigating non-V600E BRAF-driven NSCLC and evaluating MAPK pathway-targeted interventions. The table below summarizes the key biological and technical attributes of the NCI-H1755 cell line.

Our Services

Alfa Cytology provides fully integrated NCI-H1755 xenograft model services customized to your preclinical research needs. Our scientific team oversees every phase—from authenticated cell line expansion and mycoplasma screening to tumor inoculation, randomized cohort allocation, compound dosing, and comprehensive endpoint analysis—ensuring regulatory compliance, data traceability, and transparent reporting throughout your study.

Workflow of NCI-H1755 Xenograft Model Construction

Construction of the NCI-H1755 xenograft model follows a systematic, quality-assured workflow designed to ensure reproducible tumor growth, ethical compliance, and robust data generation. Each stage is executed under GLP-aligned standard operating procedures with full documentation and batch traceability from cell banking to final report delivery.

1. Cell Line Authentication and Expansion: NCI-H1755 cells are revived from authenticated cryopreserved master stocks and expanded under sterile conditions. Short tandem repeat (STR) profiling, mycoplasma testing, and viability assessment are performed to confirm identity and purity. Given the mixed growth pattern, careful attention is paid to maintaining both adherent and suspension subpopulations during expansion.
2. Animal Preparation and Cohort Randomization: Immunodeficient mice are quarantined and acclimated for a minimum of five days under controlled environmental conditions. Animals are randomized into vehicle and treatment groups based on body weight, with all protocols approved by the institutional animal care and use committee (IACUC).
3. Tumor Cell Inoculation: A suspension of 3–5 × 10⁶ NCI-H1755 cells in 100 µL of ice-cold PBS or PBS/Matrigel (1:1) is injected subcutaneously into the right flank of each mouse using a sterile 25-gauge needle. Orthotopic lung implantation is available upon request for studies requiring organ-specific tumor microenvironment interactions.
4. Longitudinal Tumor Monitoring: Tumor dimensions are measured with digital calipers twice weekly beginning from the appearance of palpable masses. Tumor volume is calculated using the modified ellipsoid formula: length × (width)² / 2. Body weight and clinical observations are recorded concurrently to assess treatment tolerability.
5. Test Article Administration: Investigational compounds are administered according to the study-specific regimen via oral gavage, intraperitoneal, intravenous, or subcutaneous routes. Vehicle control groups receive the equivalent formulation without active agent. Combination arms are configured as specified in the study protocol.
6. Endpoint Assessment and Tissue Collection: Mice are humanely euthanized upon reaching the predetermined endpoint—typically when tumor volume approaches 1,500 mm³ or at a fixed study duration. Tumors are excised, weighed, and subdivided for formalin-fixed paraffin-embedded (FFPE) histology, snap-frozen molecular analysis, and single-cell dissociation for flow cytometry.
7. Data Analysis and Study Reporting: Tumor growth curves, tumor growth inhibition (TGI) percentages, and statistical comparisons between treatment groups are generated using validated biostatistical platforms. A comprehensive study report including raw data, methodology, representative images, and mechanistic interpretation is delivered to the sponsor.

Fig 2. NCI-H1755 xenograft model construction workflow.

Case Study-NCI-H1755 Xenograft Model Development

In a recent preclinical program, the NCI-H1755 xenograft model was employed to evaluate the anti-tumor efficacy of a pan-RAF inhibitor in combination with a MEK inhibitor for BRAF Class II-mutant NSCLC. Following subcutaneous inoculation of 5 × 10⁶ cells into athymic nude mice, measurable tumors were established within 18 days with a take rate exceeding 90%. Animals were randomized into vehicle, monotherapy, and combination treatment arms once mean tumor volume reached approximately 200 mm³. Longitudinal monitoring revealed dose-dependent tumor growth inhibition across treatment cohorts, with the combination arm demonstrating superior suppression compared to either monotherapy alone. Endpoint pharmacodynamic analysis showed marked reduction of phosphorylated ERK1/2 and downstream effectors including DUSP6 and EphA2 in tumor lysates from combination-treated animals. Histopathological examination confirmed preserved adenocarcinoma morphology with reduced Ki-67 proliferative indices in responder groups. These preclinical findings supported the mechanistic rationale for advancing the combination regimen into subsequent IND-enabling studies.

Why Choose Alfa Cytology?

Engaging Alfa Cytology for your NCI-H1755 xenograft studies grants access to a scientifically rigorous, operationally transparent preclinical platform. Our integrated service infrastructure is designed to deliver high-fidelity, actionable data within competitive timelines.

• Authenticated cell repositories with routine STR profiling and mycoplasma screening to ensure genetic fidelity and experimental reproducibility.
• Customizable study designs including subcutaneous, orthotopic, and metastatic model configurations tailored to your mechanistic and therapeutic questions.
• Real-time tumor growth tracking via digital calipers or optional non-invasive imaging modalities such as bioluminescence and micro-CT upon request.
• Comprehensive endpoint analysis spanning histopathology, immunohistochemistry, Western blot, qPCR, RNA sequencing, and multiplex cytokine profiling.
• Dedicated project scientists providing weekly progress updates, direct raw data access, and regulatory-compliant documentation packages.
• Streamlined study execution with standard tumor establishment and treatment phases typically completed within 5–7 weeks from project initiation.

Contact Us

Ready to advance your BRAF Class II-targeted NSCLC research with a validated NCI-H1755 xenograft model? Reach out to the Alfa Cytology scientific team today to discuss your study design, receive a customized proposal, and discover how our preclinical expertise can accelerate your therapeutic development. Contact us now to schedule a consultation and move your program forward with confidence.

For research use only. Not intended for any clinical use.