N1E-115 Syngeneic Model Service for Neuroblastoma

The N1E-115 syngeneic model is the adrenergic heir of the C-1300 — the first transplantable neuroblastoma ever characterized — engrafting a fourteen-receptor, differentiation-competent murine neuroblastoma into syngeneic A/J hosts where immunocompetent immunotherapy evaluation meets a half-century of neurobiology. Alfa Cytology delivers this historic model as a complete preclinical service — authenticated cell banking from the 1972 reference, subcutaneous implantation in A/J hosts, surrogate-immuno-oncology efficacy and immuno-pharmacodynamic profiling, and full histopathology — giving sponsors the most pharmacologically annotated neuroblastoma platform in existence.

Overview of N1E-115 Syngeneic Model for Neuroblastoma

N1E-115 carries perhaps the deepest pedigree of any line in this catalog. Its founding tumor, C-1300, was the first transplantable murine neuroblastoma ever described — the tumor from which the entire mouse neuroblastoma field grew — and in 1971, in the laboratory of Marshall Nirenberg, T. Amano and E. Richelson cloned it and selected the adrenergic subclone N1E, from which N1E-115 was isolated by single-cell subcloning on glass shards; the characterization appeared in the Proceedings of the National Academy of Sciences in 1972. The line's biology is that of a neural-crest neuroblast endowed with an extraordinary pharmacological wardrobe: it contains fourteen neurotransmitter receptors — muscarinic M1 and M2, serotonin 5-HT₃, histamine H1, adenosine, angiotensin II, bradykinin, enkephalin, glucagon, neurotensin, prostaglandin E, somatostatin, thrombin, and VIP — and expresses high tyrosine hydroxylase and acetylcholinesterase while being almost devoid of choline acetyltransferase, a definitively adrenergic phenotype. With a modal chromosome count of 192 and a doubling time near 36 hours, it grows loosely adherent in standard DMEM-based media and remains, by ATCC's own designation, a suitable transfection host for neuroscience applications.

Fig 1. Graphical abstract of the NECTIN2-TIGIT axis study: combined anti-TIGIT and anti-PD-L1 blockade remodels the tumor microenvironment—expanding CD8+ T cells and CD11b+ myeloid cells—and induces complete responses in the N1E-115 syngeneic neuroblastoma model alongside Neuro2a and N18 models. (Wienke, Judith, et al., 2024)

Two dimensions give the line its modern utility as a tumor model. The first is differentiation competence: on DMSO, dibutyryl-cAMP, retinoic acid, serum withdrawal, or cyclin-dependent-kinase inhibition, N1E-115 cells exit the cell cycle and extend neurites into neuron-like morphology — the model system in which much of neuroblastoma differentiation biology was defined, and one with direct clinical resonance, since differentiation therapy with 13-cis-retinoic acid is a standard component of human high-risk neuroblastoma treatment. The second is immunology: N1E-115 has been validated as a syngeneic platform in A/J mice for evaluating surrogate and cross-reactive immuno-oncology agents with full immuno-pharmacodynamic profiling, and it anchored the 2024 Cancer Cell single-nucleus integrative study of neuroblastoma alongside Neuro-2a and N18 — contemporary evidence of its standing in immuno-oncology. Beyond oncology, the line serves as the canonical substrate for botulinum neurotoxin intoxication assays, acrylamide neurotoxicity comparisons, and retinoid developmental-toxicity models, making it one of the rare tumor lines whose citation record spans pharmacology, toxicology, and developmental biology in equal measure. For sponsors, N1E-115 offers a singular combination: a genuinely syngeneic neuroblastoma with defined adrenergic identity, a clinically resonant differentiation program, and the deepest receptor pharmacology of any murine tumor line.

Cell Line Information: N1E-115 Syngeneic Model

N1E-115 (ATCC CRL-2263; Cellosaurus CVCL_0451; ECACC 88112303) is the adrenergic subclone of the C-1300 spontaneous mouse neuroblastoma, established by Amano, Richelson, and Nirenberg in 1971 and characterized in PNAS 1972, distributed by the American Type Culture Collection, ECACC, and international repositories. Core characteristics are compiled below.

Our Services

Engaging Alfa Cytology for the N1E-115 syngeneic model places the most pharmacologically annotated neuroblastoma under one accountable team: authenticated, low-passage N1E-115 banks are maintained with mycoplasma-free certification and adrenergic-identity verification, syngeneic A/J hosts are sourced and acclimated, tumors are established subcutaneously at standard inocula, and treatment arms — surrogate immuno-oncology agents, differentiation-therapy modalities, or neurotoxicity-interaction studies — run through scheduled caliper monitoring and immuno-pharmacodynamic sampling to terminal histopathology with neural and immune-marker panels, all under IACUC-compliant conditions and returned as an audit-ready data package.

Workflow of N1E-115 Syngeneic Model Construction

N1E-115 studies rest on the validated subcutaneous geometry in A/J hosts, augmented where programs require it by differentiation-therapy arms exploiting the line's documented retinoid and cAMP responsiveness. A standard program proceeds as follows.

1. Cell preparation and quality control: N1E-115 cells are expanded at low passage, confirmed mycoplasma-free, and adrenergic identity spot-checked (tyrosine hydroxylase activity or receptor-expression profile); suspensions are prepared fresh at ~10⁶ cells per inoculum.
2. Host selection and acclimation: Female or male A/J mice, typically 6–8 weeks of age (the 2024 single-nucleus study deployed 6–8-week-old females), are quarantined and acclimated in a specific-pathogen-free barrier facility.
3. Implantation: subcutaneous route. 10⁶ cells in 0.1 mL sterile PBS are injected into the flank; the site is compressed briefly on needle withdrawal, and tumors establish on the expected kinetics of the C-1300 lineage.
4. Randomization and treatment. Mice are randomized by tumor volume into arms, and test articles: surrogate checkpoint inhibitors, differentiation-inducing regimens (retinoic-acid-class or cAMP-pathway modalities), targeted agents, or neurotoxicity-interaction compounds — are dosed per protocol with body weight and neurological signs recorded.
5. Differentiation-therapy arms where specified: For differentiation questions, parallel in vitro differentiation plates (DMSO, db-cAMP, or retinoic acid) accompany the in vivo arm, with neurite-outgrowth scoring anchoring mechanism claims to the line's canonical phenotype.
6. Immuno-pharmacodynamic sampling: At defined time points, tumors and blood are harvested from satellite cohorts for flow-cytometric immune profiling against the surrogate immuno-oncology panel validated for this model, and serum is banked for cytokine analysis.
7. Longitudinal monitoring: Tumors are measured by caliper on the protocol cadence; body weight and clinical signs are recorded daily, with particular attention to neurological readouts given the line's neural heritage.
8. Endpoint analysis and reporting: At termination, primary tumors are resected and weighed; tissues undergo H&E with neuroblastoma histology, immunohistochemistry (tyrosine hydroxylase, synaptophysin, CD8, CD4, FoxP3, F4/80, PD-L1 panels), and where differentiation arms are included, neuronal-marker scoring (βIII-tubulin), with all data consolidated into the final report.

Fig 2. N1E-115 Syngeneic Model construction workflow.

Case Study-N1E-115 Syngeneic Model

Alfa Cytology has applied the N1E-115 syngeneic platform to preclinical programs spanning surrogate immuno-oncology efficacy and immuno-pharmacodynamic profiling, differentiation-therapy mechanism studies, targeted-agent evaluation, and neurotoxicity-interaction questions in neuroblastoma. In these engagements, caliper readouts tracked primary tumor kinetics, satellite immuno-pharmacodynamic cohorts profiled tumor immune infiltrates by flow cytometry, and terminal histopathology with neural and immune-marker panels completed the pharmacological and biological assessment. Study parameters — inoculum, treatment arms, differentiation formats, and endpoint panels — are tailored to each program. Case materials can be shared under confidentiality agreements upon request.

Why Choose Alfa Cytology?

N1E-115 rewards teams that appreciate what it is: not merely a tumor line but a pharmacological instrument with adrenergic identity, differentiation competence, and a receptor wardrobe unmatched in murine oncology. Alfa Cytology fields the identity verification, differentiation-therapy fluency, and immuno-pharmacodynamic capabilities this line rewards, making the N1E-115 syngeneic model a distinctive asset for your neuroblastoma program.

• C-1300 first-transplantable pedigree, with the 1972 PNAS characterization as provenance anchor.
• Fourteen-receptor pharmacology, the deepest of any murine tumor line.
• Adrenergic-identity verification, with tyrosine hydroxylase spot-checks as standard.
• Differentiation-therapy fluency, from retinoic-acid to cAMP-pathway modalities with parallel in vitro arms.
• Validated A/J syngeneic geometry, consistent with the 2024 single-nucleus study deployment.
• Immuno-pharmacodynamic depth, with surrogate immuno-oncology panels and satellite-cohort sampling.
• IACUC-compliant, documentation-rich operations delivering audit-ready records throughout the study.

Contact Us

If your neuroblastoma program needs a syngeneic platform with pharmacological depth and differentiation competence, contact us today to discuss N1E-115 study design, immuno-pharmacodynamic formats, and endpoint strategy with our scientific team. Reach out for a confidential consultation and project quotation — Alfa Cytology looks forward to advancing your next preclinical study.

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