No candidate molecular target for inhalational anesthesia other than tubulin has a published model that reproduces the Meyer–Overton correlation.

This is the proponents' uniqueness claim, and it is unresolved in the strict sense: nobody has done the survey that would confirm or refute it. The only record is ORCH-E086, an assertion in a short proponent commentary, with ORCH-E084 and ORCH-E085 supplying the underlying attribution — that quantum-chemical modelling predicted the potencies of several volatile anesthetics from binding affinity at delocalized electron sites in tubulin, essentially reproducing the Meyer–Overton correlation. The primary behind that attribution is ORCH-E010, which is computational and proponent-authored and graded weak. No survey of receptor, channel or membrane models is cited, and none has been produced against it either. It is featured because it is the load-bearing premise of the case's strongest unanswered argument, and because ORCH-E031 makes the surrounding claim of a gap in the conventional account credible.

This assertion originates from an opinion commentary by Wiest without a comprehensive, systematic survey of the molecular modeling literature across competing anesthetic targets. Numerous classical models historically correlate anesthetic potency at hydrophobic pockets within ion channels and lipid bilayers to the Meyer–Overton rule. The strongest opposing consideration is that Craddock et al. specifically published a quantum chemical calculation demonstrating that volatile anesthetic binding affinity to tubulin terahertz dipole sites reproduces clinical potency.

The claim is a sweeping negative existence statement whose only ledger support is one sentence in a proponent commentary asserting "This cannot be said for any other candidate molecular target" with no survey cited — the record itself flags the uniqueness as asserted rather than demonstrated. Verifying it would require the systematic search no record in this packet performed. Under-sourced in both directions; unresolved.

The only pertinent ledger material is a proponent commentary asserting that no other candidate target reproduces Meyer–Overton, with no systematic survey supporting that universal existence claim. The underlying tubulin study is computational and may motivate a prospective test, but it cannot establish uniqueness across all published target models. The strongest opposing consideration is that the claimed tubulin potency correlation is specific and testable, even though it remains unvalidated experimentally.

The uniqueness claim appears as an assertion in proponent commentary that tubulin quantum-chemical modelling reproduces Meyer–Overton and that this “cannot be said for any other candidate molecular target,” without a cited systematic survey of failed models for other targets in the ledger. Strongest opposing consideration is that Craddock et al. 2017 do offer a concrete tubulin potency-correlation model worth prospective test, which is real work even if uniqueness is unproven.

Held on one commentary sentence with no survey behind it; no admitted evidence record is attached. Nothing in the record refutes it either: no rival target-level Meyer–Overton model appears. The related modelling (ORCH-E010) is attached to ORCH-C011, not to this claim.