Background: Malignant melanoma is characterized by molecular heterogeneity, adap-tive signaling, and limited durability of therapeutic responses. This exploratory study examined a chemically characterized dual-oil formulation composed of cold-pressed Prunus dulcis oil and Pinus sylvestris needle essential oil as an integrated life-science model linking formulation chemistry, comparator-context molecular docking, and cel-lular viability. Methods: GC-MS/FAME profiling defined the principal formula-tion-associated markers. Docking was used to prioritize structurally plausible interac-tions across a melanoma-relevant target panel, while Neutral Red Uptake assays quan-tified 24-h viability in B16F10 melanoma cells and MRC-5 fibroblasts. Spearman rank analysis was applied to the concentration–viability series to test monotonic biological coherence; a direct component-level docking-to-cellular correlation was prospectively evaluated for estimability. Results: The combined formulation yielded estimated IC50 values of 1.42% in B16F10 cells and 4.85% in MRC-5 cells (selectivity index, 3.41). Across the complete concentration range, the relationship was non-monotonic (B16F10: ρs = −0.429, p = 0.289; MRC-5: ρs = −0.381, p = 0.352), whereas the descending high-dose branch (≥0.37% v/v) showed strong inverse rank associations (B16F10: ρs = −1.000, p < 0.001; MRC-5: ρs = −0.900, p = 0.037). A statistically valid direct in silico–in vitro Spear-man coefficient could not be calculated because compound-resolved cellular pheno-types were unavailable for the six docked chemical markers. Conclusions: The data support a biologically coherent, concentration-dependent cytotoxic phenotype within the descending exposure range and define a rigorous framework for future com-pound-matched computational–experimental validation. The study should be inter-preted as hypothesis-generating rather than as evidence of cellular target engagement or therapeutic efficacy.

Background: Malignant melanoma remains a biologically aggressive cancer in which pathway redundancy and adaptive signaling can complicate durable therapeutic control. The working hypothesis is based on the following testable question: whether an archived dual-oil formulation composed of cold-pressed Prunus dulcis oil and Pinus sylvestris oil, in which α-pinene is the major component, generated a measurable NRU viability phenotype in B16F10 melanoma cells that justified subsequent standardized chemical, mechanistic, and statistical follow-up. Methods: Comparator-context docking observations were generated across a melanoma-relevant target panel, and the computational layer was used only to organize qualitative pocket-context hypotheses. The archived NRU dataset was then descriptively evaluated in B16F10 melanoma cells and MRC-5 fibroblasts. Results: The NRU data indicate an observable concentration-associated reduction in B16F10 viability for the combined formulation; and IC50/selectivity-index values were estimated from fitted dose-response curves; however, the absence of complete replicate-level raw metadata and confidence intervals requires cautious exploratory interpretation. Conclusions: The results support the cautious interpretation that a dual-oil P. dulcis and P. sylvestris formulation may serve as a pilot, hypothesis-generating anti-melanoma exploratory platform. The principal value of the study is to define the minimum experimental program required for future validation, including GC-MS batch standardization, orthogonal viability assays, replicated dose-response modeling, biochemical target assays, pathway readouts, and in vivo evaluation where justified. GC-MS/FAME profiling is incorporated as a chemical-standardization anchor for the dual-oil system. GC/MS analysis was performed to characterize the chemical profiles of cold-pressed P. dulcis oil and P. sylvestris needle essential oil, supporting chemical standardization of the dual-oil system.

Background: Previous studies have examined bioactive constituents of Prunus dulcis oil, Pinus sylvestris essential oil, and related phytochemical matrices separately; however, their combined chemical profile, comparator-context molecular-docking landscape, and comparative cellular response in melanoma and non-malignant fibroblast models remain insufficiently characterized. Methods: The analyzed study samples were profiled by GC/MS and GC/FID-based fatty-acid methyl ester analysis. An archived molecular-docking dataset was used to summarize structurally plausible interactions of six formulation-associated markers with eight melanoma-relevant or melanoma-adjacent targets and to present representative three-dimensional complexes. Because complete protocol metadata and co-crystallized-ligand redocking records were unavailable, the computational findings were interpreted descriptively. Neutral-red uptake assays assessed the 24 h viability of B16F10 melanoma cells and MRC-5 fibroblasts after exposure to each oil, the dual-oil formulation, or cisplatin. Four-parameter logistic models provided estimated IC₅₀ values, and exact two-sided permutation tests were used for Spearman rank analyses. Results: The dual-oil formulation yielded estimated IC₅₀ values of 1.42% v/v in B16F10 cells and 4.85% v/v in MRC-5 cells, corresponding to an apparent selectivity index of 3.41. The complete eight-concentration series was non-monotonic and showed no significant rank association (B16F10: ρs = −0.4286, exact p = 0.2992; MRC-5: ρs = −0.3810, exact p = 0.3599). In a post hoc analysis of the descending branch (≥0.37% v/v), the association was perfect in B16F10 cells (ρs = −1.0000, exact p = 0.0167) but did not reach significance in MRC-5 cells (ρs = −0.9000, exact p = 0.0833). The docking matrix identified target-dependent numerical prioritization patterns; however, small score differences were not interpreted as evidence of stronger binding or cellular target engagement. Conclusions: The findings define an exploratory chemical–computational–cellular framework and a preliminary formulation-level viability phenotype. They do not establish synergy, apoptosis, pathway modulation, therapeutic efficacy, or clinical safety. Independent multi-batch chemical confirmation, a fully documented and redocking-validated computational protocol, expanded melanoma and normal-skin cell panels, orthogonal functional assays, longer exposure periods, mechanistic validation, and subsequent in vivo studies are required.