# Max Goulazian

- **Event:** [Built with Claude: Life Sciences](https://cerebralvalley.ai/e/built-with-claude-life-sciences)
- **When:** Jul 7 at 12:00 PM – Jul 14 at 12:00 AM (EDT)
- **Where:** Online
- **Team:** [Max Goulazian](https://cerebralvalley.ai/u/maxgoula)
- **GitHub:** https://github.com/maxgoulazian/Spatial-ScRNA-seq-PBPK-QSP-Model.git
- **Gallery:** https://cerebralvalley.ai/e/built-with-claude-life-sciences/hackathon/gallery
- **Page:** https://cerebralvalley.ai/e/built-with-claude-life-sciences/hackathon/gallery/272

Target to a designed binder in one week.
The full immuno-oncology discovery arc — target ID, a genome-scale counter-screen, a 1.65M-edge network, a whole-body QSP model, and de novo protein design — that normally takes a multidisciplinary team 1–4.5 years, run by one scientist directing Claude. ≈60–270× faster.

CD3 T-cell engagers deliver signal 1 but no costimulation, so responses exhaust and fade. Adding a CD28 or 4-1BB arm fixes that — but because the engager grips CD3 on every T cell, it amplifies the CD4 programs that drive cytokine-release syndrome and expand suppressive Tregs. Which costim arm boosts killing without feeding toxicity?

We answer it mechanistically. We turned the Marson/Pritchard genome-scale CD4⁺ CRISPRi Perturb-seq screen into a three-axis scoring instrument — effector benefit (from a matched CD8 screen), Treg/IL-10 suppression liability, and CRS-cytokine liability — then fed all three into a whole-body single-cell spatial PBPK/QSP model: 21 tissues gridded at real single-cell resolution (~1.9M cells), every cell an agent running Rhoden bivalent binding kinetics, mechanistic per-myeloid IL-6 with zero fitted scale, validated against 20+ clinical engagers.

The verdict: 4-1BB and CD27 co-lead; CD28 is gated out on CRS and Treg liability. We then in-silico-designed binders (RFdiffusion→ProteinMPNN→AlphaFold3) against the winners — a bench-ready next step.

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