banner
Custom In Vivo Tumor Model Services
Online Inquiry

NCI-H1373 Xenograft Model Service for NSCLC

Fig 1: NCI-H1373 xenograft model for NSCLC preclinical research.

The NCI-H1373 xenograft model represents a well-established preclinical platform for interrogating KRAS-mutant non-small cell lung cancer (NSCLC), offering researchers a reproducible system to evaluate tumor growth kinetics, therapeutic response, and resistance mechanisms in an immunodeficient host environment. Alfa Cytology delivers comprehensive NCI-H1373 xenograft model services encompassing cell line authentication, tumor establishment, compound administration, and multi-parameter endpoint analysis, enabling you to generate robust, publication-ready data that advance your oncology pipeline.

Overview of NCI-H1373 Xenograft Model for NSCLC

The NCI-H1373 cell line was established in 1986 from a Stage 3A lung adenocarcinoma resected from a 56-year-old male patient and is classified as a well-differentiated pulmonary adenocarcinoma with epithelial morphology. Genetically, this line harbors a KRAS G12C activating mutation—a driver alteration present in approximately 25% of lung adenocarcinomas—along with inactivating mutations in ATM and TP53, rendering it highly relevant for investigating oncogenic signaling networks and targeted intervention strategies. When implanted into immunodeficient mice, NCI-H1373 cells form palpable, measurable tumors with consistent take rates, providing a physiologically relevant microenvironment for studying KRAS-dependent tumor biology and therapeutic vulnerabilities.

Fig 2: Reference figures for NCI-H1373 cell-related literature.Fig 1. The X-ray co-crystal structure of ASP6918 bound to KRAS G12C, together with NCI-H1373 potency readouts (pERK IC50 0.0037 μM; viability IC50 0.0061 μM), underpinned its antitumor activity in the NCI-H1373 xenograft model. (Imaizumi, Tomoyoshi, et al., 2024)

In vivo, the NCI-H1373 xenograft model has been extensively leveraged to assess the efficacy of KRAS G12C covalent inhibitors, MEK pathway blockers, and combination regimens, with tumor growth inhibition often correlated to downstream biomarker modulation such as suppression of phosphorylated ERK1/2 and S6 ribosomal protein. The model supports longitudinal caliper-based tumor volume tracking as well as advanced pharmacodynamic sampling, and harvested tumor tissues are suitable for immunohistochemistry, Western blotting, RNA sequencing, and flow cytometric analysis. These characteristics make the NCI-H1373 xenograft an indispensable tool for preclinical validation of KRAS-directed and combination therapies in NSCLC.

Cell Line Information: NCI-H1373

NCI-H1373 is a human lung adenocarcinoma cell line with well-characterized molecular alterations and robust tumorigenic potential in immunodeficient murine hosts. Established from a primary tumor specimen, this line retains epithelial morphology and expresses markers consistent with pulmonary adenocarcinoma differentiation. The table below summarizes the key biological and technical attributes of NCI-H1373 relevant to xenograft model construction.

Parameter Details
Cell Line Name NCI-H1373
ATCC Catalog No. CRL-5866
Tumor Origin Primary lung adenocarcinoma (Stage 3A)
Histological Classification Well-differentiated pulmonary adenocarcinoma
Species Human (Homo sapiens)
Age / Gender / Ethnicity 56-year-old male, Black
Patient History Smoker (30 pack-years); received prior chemotherapy and radiation therapy
Morphology Epithelial-like; adherent monolayer
Culture Medium RPMI 1640 supplemented with 10% fetal bovine serum (FBS) and 1% penicillin/streptomycin
Key Molecular Features KRAS G12C missense mutation; ATM p.E2943Ter stop-gain mutation; TP53 p.E339Ter stop-gain mutation; EGFR expression; moderate c-MET expression; high P-cadherin expression
Doubling Time Approximately 28 hours under standard culture conditions
Tumorigenicity High; forms reproducible subcutaneous tumors in athymic nude mice within 14–21 days
Recommended Inoculum 3–5 × 10⁶ cells per mouse in 100 µL PBS/Matrigel mixture (1:1)
Host Strain Athymic nude mice (nu/nu) or NOD/SCID mice, 6–8 weeks old, male or female
Tumor Growth Characteristics Moderate growth rate; mean tumor volume doubling time approximately 5–7 days
Endpoint Tumor Volume Typically 1,000–1,500 mm³ or per institutional animal welfare guidelines
Applications KRAS G12C inhibitor screening, MEK/ERK pathway evaluation, combination therapy assessment, pharmacokinetic/pharmacodynamic studies, biomarker validation, ADC efficacy testing

Our Services

Alfa Cytology offers fully customizable NCI-H1373 xenograft model services designed to accelerate your preclinical oncology research. From initial cell line expansion and mycoplasma testing to randomized group allocation, compound dosing, and comprehensive endpoint analysis, our experienced scientific team ensures that every study is executed with precision, regulatory alignment, and transparent reporting—delivering actionable data you can trust.

Workflow of NCI-H1373 Xenograft Model Construction

Construction of the NCI-H1373 xenograft model proceeds through a standardized, quality-assured workflow that ensures reproducible tumor growth, ethical compliance, and data integrity. Each phase is documented under GLP-aligned standard operating procedures with full traceability from cell banking to final report delivery.

  1. Cell Line Expansion and Authentication: NCI-H1373 cells are revived from authenticated cryopreserved master stocks and expanded under sterile conditions. Short tandem repeat (STR) profiling and mycoplasma testing are performed to confirm identity and purity before inoculation.
  2. Animal Acclimation 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. Subcutaneous Tumor Cell Inoculation: A suspension of 3–5 × 10⁶ NCI-H1373 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.
  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.
  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 matched formulation without active agent.
  6. Endpoint Tissue Collection and Processing: 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 suspension for flow cytometry.
  7. Data Analysis and Study Reporting: Tumor growth curves, tumor growth inhibition (TGI) percentages, and group-wise statistical comparisons are generated using validated biostatistical platforms. A comprehensive study report including raw data, methodology, representative images, and interpretation is provided to the sponsor.

Fig 3: Workflow for the establishment of NCI-H1373 cell line–derived xenograft (CDX) models.Fig 2. NCI-H1373 xenograft model construction workflow.

Case Study-NCI-H1373 Xenograft Model Development

In a recent preclinical program, the NCI-H1373 xenograft model was utilized to evaluate the anti-tumor activity of a novel KRAS G12C-targeted therapeutic candidate. Following subcutaneous inoculation of 5 × 10⁶ cells into athymic nude mice, measurable tumors were established within 16 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. Dose-dependent tumor growth inhibition was observed across treatment cohorts, with responder groups showing marked suppression of phosphorylated ERK1/2 and Ki-67 proliferative indices in excised tumor tissues. Pharmacokinetic sampling confirmed compound exposure correlated with pharmacodynamic response, supporting the advancement of the candidate into subsequent IND-enabling toxicology studies.

Fig 4: Case Study-NCI-H1373 Xenograft Model Development.

Why Choose Alfa Cytology?

Selecting Alfa Cytology as your partner for NCI-H1373 xenograft studies ensures access to a scientifically rigorous, operationally transparent preclinical infrastructure. Our integrated service model is designed to deliver high-fidelity data within competitive timelines.

  • Routinely authenticated cell banks with STR profiling and mycoplasma screening to preserve genetic fidelity throughout the study.
  • Flexible model configurations including subcutaneous, orthotopic, and metastatic dissemination formats tailored to your mechanistic questions.
  • Real-time tumor growth tracking via digital calipers or optional non-invasive imaging modalities such as bioluminescence and micro-CT.
  • Comprehensive endpoint portfolios spanning histopathology, immunohistochemistry, Western blot, qPCR, RNA-seq, and multiplex cytokine analysis.
  • Dedicated project scientists providing weekly progress updates, direct access to raw datasets, and regulatory-compliant documentation packages.
  • Streamlined study execution with typical tumor establishment and treatment phases completed within 5–7 weeks from project initiation.

Contact Us

Ready to advance your KRAS-directed NSCLC research with a validated NCI-H1373 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.

Reference

  1. Imaizumi, Tomoyoshi, et al. "Discovery of ASP6918, a KRAS G12C inhibitor: Synthesis and structure–activity relationships of 1-{2, 7-diazaspiro [3.5] non-2-yl} prop-2-en-1-one derivatives as covalent inhibitors with good potency and oral activity for the treatment of solid tumors." Bioorganic & Medicinal Chemistry 98 (2024): 117581.

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

Related Services

Adrenal Cancer
Breast Cancer
Biliary Tract Cancer
Head and Neck Cancer
Bladder Cancer
Cervical Cancer
Glioblastoma
Retinoblastoma
Medulloblastoma
Colon Cancer
Endometrial Cancer
Gastric Cancer
Epidermoid Carcinoma
Esophageal Adenocarcinoma (EAC)
Esophageal Squamous Cell Carcinoma (ESCC)
Ewing's Sarcoma
AML
CML
ALL
Leukemia
Liver Cancer
Prostate Cancer
NSCLC
Large Cell Carcinoma