Congenital factor XIII deficiency (F13A1) OMIM 613225

In Congenital factor XIII deficiency (F13A1, OMIM 613225), the master switch sits on the ↓ DOWN branch ([F] forced below); the healthy state is the ON well. The forced corrective direction is to raise s toward ON branch (polarity: supply). Classification: ✓ Recovers an existing standard. Direction only — no dose, no efficacy magnitude.

The disease maps to an R19 double-well whose corrective lever is read straight off the cusp (barrier 0.4947, γ 1.4067, spinodal 0.6422). The corrective direction is forced [F]; the agent names below are direction-concordant labels at grade [O] (no dose, no efficacy or safety magnitude). This is a research hypothesis offered to experts, not medical advice.

The emergence switch

The switch for Congenital factor XIII deficiency is an R19 double-well emerged from the real proximal-promoter DNA of F13A1. Its geometry is fixed by measured stiffness γ (never fitted); the numbers below are read directly off that cusp.

emergent axis
↓ DOWN [F]
healthy branch
ON
lesion
LOF_null
γ (stiffness)
1.4067
barrier
0.4947
spinodal
0.6422
s_on / s_off
1.1860 / -1.1860
fragility
0.48
corrective polarity
supply
forced direction
raise s toward ON branch

Chemistry feasibility (DIRECTION only [O]). small-molecule recrossing of the fold is geometrically plausible (barrier 0.4947 at neutral drive; lower barrier = smaller drive to supply). [O] -- no affinity/potency/dose/efficacy asserted.

The derived corrective lever

The cusp forces a corrective direction: raise s toward ON branch. This is the load-bearing output of the framework — it is [F] forced, and it is falsifiable. 2 lever families are derived; the lead is h-restore (drive modulator).

h-restore (drive modulator)sign: increasegeometric rank 0.48
Mechanism. supply / restore the positive drive (replace-or-agonise the missing competence)
Applies to. allele-agnostic (downstream/environmental tilt)
favoured when the switch is fragile -- a small drive shift recrosses the fold
Falsifier. If supplying/agonising fibrin-stabilising factor XIII activity (raising the switch drive) does NOT move the DOWN [F] switch toward the healthy branch in a F13A1-deficient model, the h-restore(supply) lever is refuted for this axis.
gamma-restore (stabiliser / chaperone)sign: Nonegeometric rank 0.00
Mechanism. N/A
Applies to. none (honest exclusion)
EXCLUDED: null allele -- no product to stiffen
Falsifier. If a folding-stabiliser/chaperone does NOT re-deepen the healthy well for a residual F13A1 allele (no rescue that a null allele lacks), the gamma-restore lever is refuted; null alleles are excluded by construction.

Agents mapped onto the lever

✓ Agreement with established practice. The corrective direction derived here (raise s toward ON branch) independently matches an agent already in clinical use for this disease: factor XIII concentrate (catridecacog / recombinant FXIII-A2; plasma-derived FXIII). The geometry recovered known medicine — this is a validation signal for the logic, not a new treatment claim by this kit.
Existing agents whose known action is direction-concordant with the derived lever (status as pinned in the corpus; no dose, no efficacy magnitude).
agent (class)dir.statusphasemap
factor XIII concentrate (catridecacog / recombinant FXIII-A2; plasma-derived FXIII)
Ichinose 1986 Biochemistry 25:6900; Inbal 2012 Blood 119:5111
increaseapproved4✓ in use
⚠ Mechanism-direction only — do not self-administer; no dose (unvalidated; set by a physician / national authority); not an approved use.

Direction-only candidate leads (corpus join)

Each lead is surfaced only because its known mechanism points the same way as the derived lever, and each comes with a source and a falsifier. None is a treatment.

factor XIII concentrate (catridecacog / plasma-derived FXIII) [FXIII deficiency]✓ recovered standarddir: increase · approved
Class. coagulation factor XIII replacement (fibrin cross-linking)
Mechanism. F13A1 loss removes fibrin-stabilising factor XIII activity; a factor XIII concentrate replaces it, restoring clot cross-linking. Direction: increase / supply the deficient factor. Allele scope: agnostic. Gene-specific to F13A1.
✓ This is a rediscovery. Factor XIII concentrate is approved for congenital factor XIII deficiency; recovered by the direction logic.
Safety (qualitative; no magnitude). post-marketing safety profile on record (approved factor concentrate; qualitative; no magnitude)
Falsifier. If factor XIII concentrate (catridecacog / plasma-derived FXIII) [FXIII deficiency] (a gene-specific supply/increase agent) does NOT move the DOWN [F] switch toward the healthy branch in a F13A1-deficient model, the h-restore(supply) direction is refuted for factor XIII concentrate (catridecacog / plasma-derived FXIII) [FXIII deficiency] here.
Source: FDA/EMA label: factor XIII concentrate for congenital FXIII deficiency
⚠ Mechanism-direction only — do not self-administer; no dose (unvalidated; set by a physician / national authority); not an approved use.

Evidence & provenance

What is reproduced vs. cited for this page.
elementgradebasis
R19 switch & cusp geometry (this page)[V] verifiedemerged from measured promoter γ of F13A1; deterministic, 2×sha256 identical
corrective direction[F] forcedforced by the cusp sign; falsifiable (see lever falsifiers)
mapped agents / leads[O] opendirection-concordance only; corpus-pinned (2026-06-21); no dose, no efficacy/safety magnitude

Reading the agent column. VALIDATION SIGNAL -- the agent is already approved / established standard for this disease, so the direction logic recovered known clinical practice. Not a new claim by this kit. GENUINE HYPOTHESIS -- no approved indication for this disease; the direction match is a direction-only, untested [O] lead. Basis field grades the evidence (investigational here / in a related condition / off-label / speculative).