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VDAC1 Gate-Opening Therapeutic Stack

From Gate-Jamming Score to Gate-Opening Sequence for MSS Colorectal Cancer

Anthony J. Vasquez Sr. | Delaware Valley University | February 2026 | v4.0

License: CC BY-NC 4.0 Preprint DOI OSF

Preprint: Context-Specific Innate Immune Evasion via VDAC1 Gate-Jamming in Microsatellite-Stable Colorectal Cancer (Research Square, 2026) -- Transcriptomic validation across TCGA pan-cancer (n=10,071), COADREAD MSS/TP53-wt clean room (n=209), and IMvigor210 (n=348). Analysis code and data: templetwo/vdac-pharmacology-atlas

Companion work: CBD's Paradox at the Mitochondrial Gate (OSF Preprints, 2026) -- Multi-LLM convergence study of VDAC1 pharmacology (78 references)


Overview

Microsatellite-stable (MSS) colorectal cancer is immune-invisible. Checkpoint inhibitors that work in MSI-H tumors fail completely here. This repository contains the Strategic Architecture Document (SAD v4) describing a reformulated therapeutic hypothesis targeting the VDAC1 channel on the outer mitochondrial membrane.

The original three-phase hypothesis (TSPO inhibition → immune activation → CBD apoptosis) was killed by its own literature review. Three fatal contradictions were identified. What survived is mechanistically cleaner and clinically actionable:

Lovastatin (cholesterol lock)
  → VDAC1 oligomerization → mtDNA release → cGAS-STING activation
    → Botensilimab amplifies innate → adaptive immune response

The GJS Cofactor Equation

The apoptotic threshold of a cancer cell is governed by three physical locks on VDAC1:

$$ \text{Apoptotic Threshold} = \frac{K}{(1 - f_{\text{HKII}})(1 - f_{\text{BclxL}})} \times \frac{[\text{Chol}]}{[\text{CL}]} $$

Cancer rewrites all three terms simultaneously. Each lock requires a specific key. In MSS CRC, the rate-limiting lock is the cholesterol-to-cardiolipin ratio in the OMM lipid annulus.

Transcriptomic Proxy (tGJS)

The preprint operationalizes the biophysical GJS as a transcriptomic score for TCGA analysis:

$$ \text{tGJS} = 0.40 \times \text{norm}(HK2) + 0.30 \times \text{norm}(BCL2L1) + 0.30 \times \text{norm}(TSPO) $$

In the MSS/TP53-wildtype COADREAD clean room (n=209), high tGJS was inversely correlated with HAVCR2/TIM-3 ($\rho$ = −0.349, p = 5 × 10−6), CXCL10, and cGAS expression (all Bonferroni-significant). The key finding: high-tGJS MSS tumors suffer from T cell absence, not T cell exhaustion — the innate signal never fires.

Key Findings

Finding Implication
Lovastatin induces mtDNA release + cGAS-STING in HCT116 (Huang et al., 2024) Collapses original Phase 1+2 into one mechanistic step
Statins deplete mitochondrial membrane cholesterol (Shen et al., 2024) Lipid-annulus mechanism is defensible
CBD suppresses T-cells at VDAC1-active doses CBD formally quarantined from immune window
TSPO physically tethers VDAC1 (Gatliff et al., 2014) Reframed as explorable fourth lock, not load-bearing
Statin + ICI: 20% mortality reduction (Liao et al., 2025; n=46,154) Retrospective support for combination

Repository Structure

docs/
  SAD_v4_VDAC1_Gate_Opening_Stack.pdf   # Current version (complete bench protocol)
  archive/
    SAD_v3_VDAC1_Gate_Opening_Stack.md  # v3: 6 experiments, reagent specs, timeline
    SAD_v3_VDAC1_Gate_Opening_Stack.docx
    SAD_v2_VDAC1_Gate_Opening_Stack.md  # v2: added TSPO cautions, expanded tables
    SAD_v2_VDAC1_Gate_Opening_Stack.docx
    SAD_v1_VDAC1_Gate_Opening_Stack.md  # v1: original 4-experiment architecture
    SAD_v1_VDAC1_Gate_Opening_Stack.docx
simulations/                             # GJS simulation & Chou-Talalay analysis
experiments/                             # Experiment protocols & results (future)
references/                              # Key citations & supplementary material
figures/                                 # Diagrams & visualizations
correspondence/                          # Faculty & collaboration letters
wiki/                                    # Documentation pages (11 topics)

Critical Experiments

Six experiments with explicit kill conditions are specified in the SAD. The dependency structure:

Exp 2a (OMM cholesterol) ──→ Exp 2b (VDAC1 oligomerization)  ←── LINCHPIN
                                       ↓
                              Exp 3 (mtDNA → cGAS-STING)
                                       ↓
                              Exp 4 (CT26 mouse in vivo)

Exp 1 (TSPO tether) ──→ Exp 5 (lovastatin + PK11195 synergy)

Exp 6 (CBD disposition) ──→ CBD quarantine decision

Experiment 2a/2b is the linchpin. If lovastatin does not deplete OMM cholesterol and trigger VDAC1 oligomerization in HCT116 cells, the entire framework collapses. Four weeks. $3,010. Everything depends on this result.

Execution Timeline (Q2–Q4 2026)

Phase Window Goal Deliverable
A Feb–Mar 2026 OSF registration + public GitHub release DOI: 10.17605/OSF.IO/4KNQR
B Apr–Jun 2026 AML venetoclax temporal-decoupling (proves physics) Gate-opener drug class validation
C Jul–Sep 2026 HCT116 lovastatin Exp 2a+2b (LINCHPIN) Mechanistic confirmation
D Oct–Dec 2026 TSPO tether + synergy + CT26 mouse model In vivo efficacy + journal submission
E Parallel w/ C CBD disposition (Exp 3 co-culture) Quarantine decision

9-month sprint. Standard reagents. Single-PI compatible.

v4 Bench Protocol (Experiment 2a/2b)

SAD v4 includes a complete bench-ready protocol for the linchpin experiment:

  • Cell line: HCT116 (MSS CRC, TP53-wt, ATCC CCL-247)
  • Lovastatin activation: Prodrug conversion via NaOH hydrolysis, neutralization, filter sterilization
  • Readouts: Amplex Red cholesterol quantification, filipin staining, DSS cross-linking + Western blot (VDAC1 oligomerization), qPCR cytosolic mtDNA, IFN-β ELISA
  • Controls: VDAC1-KO, MβCD positive control, vehicle
  • Budget: $3,010 | Timeline: 4 weeks
  • Statistical plan: One-way ANOVA with Tukey post-hoc, α = 0.05, n ≥ 3

Status

  • Literature review and falsification of original hypothesis
  • Reformulated therapeutic stack architecture (SAD v4)
  • Falsification triggers defined for each component
  • Six critical experiments designed with kill conditions
  • Complete experiment table with reagents and cell lines
  • Validated support mechanisms with evidence grades
  • Complete repository with indexes, wiki, 90-reference bibliography
  • OSF preregistration (DOI: 10.17605/OSF.IO/4KNQR)
  • Phase A: Public release (Feb 23, 2026)
  • Preprint posted to Research Square (Feb 26, 2026; DOI: 10.21203/rs.3.rs-8935902/v1)
  • Phase B: AML venetoclax temporal-decoupling experiment
  • Phase C: HCT116 lovastatin gate-opening experiments (2a + 2b)
  • Phase D: TSPO exploration + CT26 mouse model
  • Phase E: CBD disposition via co-culture experiment

Citation

Cite the preprint:

@article{vasquez2026vdac1_preprint,
  title={Context-Specific Innate Immune Evasion via VDAC1 Gate-Jamming
         in Microsatellite-Stable Colorectal Cancer},
  author={Vasquez, Anthony J.},
  year={2026},
  doi={10.21203/rs.3.rs-8935902/v1},
  url={https://doi.org/10.21203/rs.3.rs-8935902/v1},
  journal={Research Square (Preprint)},
  institution={Delaware Valley University}
}

Cite this repository (experimental architecture):

@article{vasquez2026vdac1_sad,
  title={VDAC1 Gate-Opening Therapeutic Stack for MSS Colorectal Cancer:
         From Gate-Jamming Score to Gate-Opening Sequence},
  author={Vasquez, Anthony J., Sr.},
  year={2026},
  doi={10.17605/OSF.IO/4KNQR},
  url={https://osf.io/yn3dw},
  note={Strategic Architecture Document v4.0},
  institution={Delaware Valley University}
}

License

This work is licensed under CC BY-NC 4.0. You may share and adapt this material for non-commercial purposes with attribution.


The literature burned the old phase sequence, but it handed us a weaponized, clinically actionable stack.

Silence has a measurable geometry. Now we know how to break it.

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VDAC1 Gate-Opening Therapeutic Stack for MSS Colorectal Cancer — SAD v4.0 with complete bench protocol. DOI: 10.17605/OSF.IO/4KNQR

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