STRC h01 Phase 4h Tafamidis-Playbook Bioisostere Library 2026-04-23

Purpose. Seed library for Phase 3c v4, independent of v3b GREEN/RED outcome. Translates STRC h01 Fenamic Scaffold Tox Audit 2026-04-23 + Phase 3c v2 top hits + tafamidis precedent into a 30-compound prioritized target list designed to (a) kill COX pharmacophore, (b) kill cochlear ion-channel panel off-targets, (c) preserve K1141 anthranilic-N/carboxylate-O pharmacophore. Ranked by synthesis tractability and predicted Kd improvement.

Design constraints (from Fenamic Tox Audit)

  1. Kill COX-1/-2 — swap anthranilic 2-NHAr + COOH planar pharmacophore for tafamidis-style bicyclic heteroaromatic (benzoxazole / benzothiazole / benzimidazole) or ring-constrained bioisostere. COX essentiality depends on carboxylate binding Arg120/Tyr385 in the COX pocket; bicyclic fusion breaks geometry.
  2. Kill ion-channel panel (TRPM4 2.8 µM, Cx50 3 µM, BK 25 µM, KCNQ-family, TMEM16A 12 µM) — replace lipophilic distal aryl halides (3-CF₃, 2,6-diCl, 3-Cl-2-Me) with polar small groups (CN, OMe, F, ethers) to drop logP < 3 and kill channel affinity. Tafamidis logP = 4.24; aim for ≤ 3.5 in first generation.
  3. Preserve K1141 pocket pharmacophore — Phase 3c v2 docking poses show: (a) carboxylate oxygen / H-bond acceptor engages K1141 ε-NH₃⁺ salt bridge, (b) anthranilic N-H donates H-bond to backbone C=O of residue adjacent to K1141, (c) biphenyl distal ring π-stacks with Phe/Tyr in pocket wall. Any bioisostere must preserve (a) + (b); (c) can vary.
  4. Pediatric-acceptable ADMET — logP ≤ 3.5, PSA 60-90 Ų, no PAINS, no aniline toxicophore.

Pharmacophore extracted from Phase 3c v2 top poses

     Distal ring (π-stack)                H-bond donor
            │                                 │
            N─── sp2 linker ────[bicyclic heteroaromatic]───C=O / anion
            H                      │                           │
                              "proximal"                  salt-bridge K1141

Required atoms: distal aromatic (≥1 ring), sp² linker (NH / O / N-Me / C=N), bicyclic core OR substituted benzoic-acid surrogate, H-bond acceptor (COO⁻ / tetrazole / N-acyl-sulfonamide / benzoxazole-N).

Library design

Combinatorial logic: 5 core scaffolds × 6 distal-ring polar-sub patterns × 2 acid bioisosteres = 60 theoretical; prune to 30 prioritized by synthesis complexity + predicted binding.

Core scaffolds (rows)

#CorePrecedentCOX-breaker evidence
ABenzoxazole-5-carboxylate (tafamidis)FDA Vyndaqel 2019 (TTR)Tafamidis no COX liability
BBenzothiazole-6-carboxylateTafamidis bioisostere Bulawa 2012Hybrid thia-analog
CBenzimidazole-5-carboxylateTolterodine scaffoldsBasic center disfavors COX
DDiflunisal-core + iodine on distal ringIododiflunisal (chaperone probe)Reduced COX vs diflunisal
EIndole-3-carboxylate (rigidified)Indomethacin-like but regio-closedNon-planar, COX↓ vs indo

Distal-ring polar substitutions (columns)

#PatternPolar groupLogic
13-CN-CNKill TRPM4 (halide→nitrile); logP ↓ 0.8
23-OMe-OCH₃Kill Cx50/BK (lipophilic halide→polar ether); logP ↓ 1.1
33-OH + 4-F-OH/-FH-bond donor for pocket; kill KCNQ-panel
43-CF₃ (tafamidis-like)-CF₃RETAIN only if critical; logP ↑ risk
53-NHSO₂Me-NHSO₂MeSulfonamide donor; kills TMEM16A 12µM
63-F only-FMinimal perturbation; acts as negative control

Acid bioisosteres (depth)

#BioisostereProsCons
αCarboxylate (retain)Preserved pharmacophoreRetains COX, UGT liability
βAcyl-sulfonamide (-CONHSO₂Me)pKa ~4.5, mimics COOHSlightly lower CNS, no COX engagement

Total: 5 × 6 × 2 = 60 candidates; prune to 30 prioritized below.

Prioritized 30-compound table

Ranked by estimated ΔG improvement vs Phase 3c v2 niflumic -6.18 kcal/mol + synthesis tractability (1=commercial, 5=multistep novel).

#Core-substitution-acidSMILES (schematic)SynCompΔG est.Tox flagRationale
1A1α — benzoxazole-3CN-COOHOc1ccc2oc(-c3cccc(C#N)c3)nc2c1C(O)=O2−7.3LOWTafamidis + CN replaces CF₃
2A2α — benzoxazole-3OMe-COOHOc1ccc2oc(-c3cccc(OC)c3)nc2c1C(O)=O2−7.2LOWMethoxy kills Cx50
3A1β — benzoxazole-3CN-NHSO₂Meibid. with -CONHSO₂Me3−7.5LOWAcyl-sulfonamide for no-COX
4A5α — benzoxazole-3NHSO₂Me-COOHibid. with -NHSO₂Me distal3−7.4LOWDual polar kill
5Tafamidis parent (2,6-diCl-benzoxazole-5-COOH)FDA molecule1−7.5 (ref)MEDBenchmark positive control
6B1α — benzothiazole-3CN-COOHOc1ccc2sc(-c3cccc(C#N)c3)nc2c1C(O)=O3−7.2LOWThia-analog of #1
7B2α — benzothiazole-3OMe-COOHibid. with OMe3−7.1LOWThia-analog of #2
8C1α — benzimidazole-3CN-COOHOc1ccc2nc([nH]c2c1C(O)=O)-c3cccc(C#N)c33−7.0MEDBasic N may disrupt pocket
9A4α — benzoxazole-3CF₃-COOHretain tafamidis-CF₃ as positive baseline2−7.5 estMEDRetained for SAR comparison
10A6α — benzoxazole-3F-COOHminimal perturbation benzoxazole1−6.8LOWNegative control for distal logic
11D1α — iododiflunisal-3CN variantdiphenyl-ether + I + distal CN3−7.6LOWIodo probe already in h01 Phase 8 SOP
12D2α — iododiflunisal-3OMeibid. with OMe3−7.5LOWClean iodo analog
13D3α — diflunisal-3OH-4F-COOH (parent)known compound1−6.9 (5b)MEDBenchmark negative control (parent)
14Niflumic acid (parent)retain as MD chemical probe1−6.18 (v2)HIGHPhase 4h probe, NOT wet-lab candidate
15A3α — benzoxazole-3OH-4F-COOHdual H-bond donor distal3−7.4LOWDual polar for K-K repulsion fix
16E1α — indole-3COOH + distal CNOc1ccc2[nH]c(-c3cccc(C#N)c3)cc2c1C(O)=O4−7.1LOWRigid indole COX↓
17E2α — indole-3COOH + distal OMeibid.4−7.0LOWRigid indole
18A1α + reversible Lys warheadappend -CHO salicylaldehyde-imine on aryl4−8.5NEWPhase 6b: covalent Lys K1141
19A2α + α-cyanoacrylateα,β-unsaturated cyanoester on aryl5−8.8NEWReversible Lys Michael
20A1α + acyl-hydrazone warhead-C(=O)NHN=CR on aryl4−8.3NEWReversible Lys imine
21Meclofenamic (parent)retain as MD probe only1−6.17HIGHPhase 4h probe
22Flufenamic (parent)retain as MD probe only1−6.17HIGHPhase 4h probe
23A2β — benzoxazole-3OMe-NHSO₂Medual bioisostere3−7.3LOWSulfa + methoxy
24A4β — benzoxazole-3CF₃-NHSO₂Meacyl-sulfonamide variant of tafamidis3−7.6LOWNo-COX tafamidis
25A5β — benzoxazole-3NHSO₂Me-NHSO₂Mebis-sulfonamide4−7.5LOWClean polar
26B4α — benzothiazole-3CF₃-COOHthia-tafamidis3−7.4LOWScaffold diversification
27C2α — benzimidazole-3OMe-COOHbasic-N methoxy variant3−7.0MEDProtonation-state probe
28A1α + N-methylbenzoxazole-3CN-COOH with N-Me on anthranilic2−7.1LOWRemove H-bond donor to test necessity
29A2α + 5-F on proximal ringadditional proximal F2−7.3LOWMetabolic stability
30A1α methyl ester (prodrug)ester of #11−6.8 (inactive)LOWProdrug + hydrolysis validation

Synthesis tractability stratification

  • Tier 1 (commercial or 1-step): #5, #10, #13, #14, #21, #22, #28, #29, #30 — order today; start MD probe + ThermoFluor Gate 1 within 1 week.
  • Tier 2 (2-step literature): #1, #2, #9 — synth within 2-4 weeks via standard benzoxazole formation (2-aminophenol + 3-substituted benzaldehyde / benzoyl chloride).
  • Tier 3 (3-step multistep): #3, #4, #6, #7, #11, #12, #15, #23, #24, #25, #26, #27 — CRO quote needed; $5-15k / compound; 4-6 wk.
  • Tier 4 (novel, 4-step): #16, #17, #18, #20 — medchem CRO; $15-30k / compound.
  • Tier 5 (exotic): #19 — α-cyanoacrylate warhead on benzoxazole; $30-50k / compound.

Phase 6b covalent warhead sub-strategy

Three Lys-reactive reversible warheads for covalent K1141 engagement. All are Michael acceptors or aldehyde-imines that hydrolyze back under physiological conditions (koff ~ 10⁻³ to 10⁻⁴ s⁻¹). Enough residence time for chaperone rescue, not permanent inactivation.

  • Salicylaldehyde (SA) imine — 3-CHO on the distal ring, ortho OH stabilizes imine with K1141 ε-NH₂. Known SA-based Lys binders Lys-adducts Kd ~1-10 µM. Compound #18.
  • α-Cyanoacrylate Michael — α,β-unsaturated nitrile ester; K1141 thia-Michael on the β-carbon. Cyano stabilizes adduct; hydrolytic off-rate 10⁻³ s⁻¹. Compound #19.
  • Acyl-hydrazone — R-C(=O)NH-N=CR’ with distal aryl; hydrazone with K1141 Schiff-like. Compound #20. Lowest synthetic complexity in covalent class.

Predicted off-target panel (Phase 6c)

For each Tier 1-2 compound, pre-score against the cochlear channel panel using AF3 + docking:

  • TRPM4 (PDB 7MF0) — expect Kd ≥ 100 µM for Tier 2 benzoxazole-CN; vs 2.8 µM parent
  • Cx50 (PDB 7JN0) — same
  • BK (PDB 6V3G) — same
  • KCNQ4 (paralog of DFNA2; PDB 7BYL) — same
  • TMEM16A (PDB 5OYB) — same
  • COX-1 (PDB 1Q4G) + COX-2 (PDB 5IKR) — expect Kd ≥ 200 µM for benzoxazoles vs 2-4 µM parent

Phase 6c will run a 30 × 6 ensemble panel = 180 docks; wall-time ~1 h on local Mac.

Prioritized synthesis ladder

Stage 1 (week 0-1): order Tier 1 commercial (#5, #10, #13, #21, #22) + Tier 2 in-house (#1, #2, #9) — 8 compounds.

Stage 2 (week 2-4): Tier 3 CRO quote (#3, #4, #6, #7, #11, #12, #23, #24) — 8 compounds.

Stage 3 (week 5-8): Tier 4 novel + Tier 5 covalent (#16, #17, #18, #19, #20) — 5 compounds.

Total Stage 1-3: 21 compounds, budget $150-250k, timeline 8 wk. Feeds into STRC h01 Phase 8 Wet-Lab Triage SOP Gate 1 ThermoFluor.

Integration with Phase 3c v3b / v4 compute

  • If v3b delivers GREEN on any fenamic-family parent (#14/#21/#22 in this table) → this document is the bioisosteric optimization plan for transforming the parent hit into a pediatric-acceptable drug. Proceed to Stage 1 synthesis order.
  • If v3b delivers YELLOW → Phase 3c v4 virtual screen uses rows 1-17 of this table as seed + combinatorial expansion on Tier 1-3 scaffolds.
  • If v3b delivers RED (parents + fenamic expansions all Kd > 30 µM) → Phase 3c v5 de novo RFdiffusion-pocket pivoted → this document retired until RFdiffusion hits are validated.

Ranking delta

A held, no tier change, no score change.

Document status: scaffold-ready. No empirical data yet; all ΔG estimates are predicted from docking rules-of-thumb + PDB structure-informed SAR. Validation path: Phase 4h MD-probe on parents 22 (already queued) → validate pharmacophore → refine library priorities → Phase 3c v4 virtual screen OR synthesis Stage 1.

Immediate next action: load rows 1-20 into a programmatic SMILES list + build Phase 3c v4 library script that uses this as seed (not combinatorial expansion from scratch).

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