SK-MEL-24 Xenograft Model

SK-MEL-24 Xenograft Model Overview

The SK-MEL-24 xenograft model is derived from the SK-MEL-24 human melanoma cell line, which was established from a metastatic lymph node biopsy of a patient with malignant melanoma. This cell line represents a classic example of BRAF-wildtype cutaneous melanoma and is widely utilized in preclinical studies focused on the development of therapies that target non-BRAF-driven melanoma pathways. SK-MEL-24 xenografts provide a reliable and biologically representative in vivo model for evaluating tumor growth kinetics, drug efficacy, and resistance mechanisms in metastatic melanoma that lacks common BRAF mutations.

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Biological and Molecular Characteristics

SK-MEL-24 cells exhibit characteristic features of amelanotic melanoma, including spindle-shaped morphology and an epithelial-like adherence pattern. Genetically, the cell line lacks BRAF V600E mutations but shows alterations in other signaling pathways such as NRAS and PI3K/AKT, making it a valuable model for assessing therapies outside the MAPK pathway. Immunophenotypically, SK-MEL-24 expresses melanoma-associated antigens including S100, HMB-45, and Melan-A/MART-1, while also exhibiting variable expression of PD-L1, a feature that enhances its utility in immuno-oncology research. The absence of pigment granules and BRAF mutations classifies this model within a distinct molecular subtype of melanoma often associated with treatment resistance.

CharacteristicDescription
Tumor OriginHuman metastatic cutaneous melanoma
BRAF StatusWildtype (non-mutated)
Antigen ExpressionS100+, HMB-45+, MART-1+
Signaling PathwaysNRAS, PI3K/AKT, limited MAPK activation
Clinical RelevanceNon-BRAF melanoma therapy development, immune modulation

In Vivo Model Development and Tumorigenicity

SK-MEL-24 xenograft tumors are typically established by subcutaneous injection of cultured cells into immunodeficient mice, such as NOD/SCID or NSG strains. Tumor initiation is observed within 2–3 weeks post-implantation, with reproducible growth kinetics and tumor volumes reaching 700–900 mm³ within 6–8 weeks. The model demonstrates a moderate growth rate, allowing for longitudinal monitoring of tumor progression and therapeutic responses. Its consistent engraftment efficiency and lack of spontaneous metastasis make it well-suited for controlled efficacy studies and pharmacodynamic analysis of single-agent or combination treatments.

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Histopathology and Immunohistochemical Profile

Histological examination of SK-MEL-24 xenografts reveals poorly differentiated, amelanotic tumors composed of spindle and epithelioid cells arranged in a disorganized pattern. The tumor cells show moderate pleomorphism, vesicular nuclei, and frequent mitotic figures, reflecting high proliferative capacity. Immunohistochemistry demonstrates robust cytoplasmic and nuclear staining for S100 protein, strong membranous expression of MART-1 and HMB-45, and variable PD-L1 expression depending on tumor microenvironmental stimuli. The Ki-67 proliferation index is typically in the range of 50–70%, supporting its use in evaluating anti-proliferative and immune-targeted therapeutics.

Preclinical Applications and Drug Response

The SK-MEL-24 xenograft model is frequently employed in preclinical research focused on therapeutic strategies for BRAF-wildtype melanoma, including inhibitors of PI3K, MEK, and mTOR, as well as checkpoint inhibitors targeting PD-1 and CTLA-4. Its responsiveness to immune modulators and targeted agents offers a flexible system for studying resistance mechanisms, particularly in melanomas that do not respond to BRAF or RAF/MEK inhibition. Furthermore, this model is applicable in combination therapy investigations that evaluate synergy between targeted agents and immunotherapeutics in a non-pigmented melanoma context.

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To request the SK‑MEL‑24 xenograft model for your preclinical studies, please use the form below. A customized quote and additional model specifications will be provided upon inquiry.

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