Company: LNAI
Filing Date: 2025-09-29
Form Type: 10-K
Source: 0001731122-25-001316
Chunk: 1116

Company: Lunai Bioworks Inc.
Filing Date: 2025-09-29
Form: 10-K
Item: Item 1
Chunk 1116
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 observations that are critical for this application. The result is both an experimental platform and coupled
computational model that can identify both neurotherapeutics and neurotoxins, the former through direct experimental screening, and the
latter through machine-learning based prediction based on chemical structure.

12

We next we examined the ability
of one of these compounds (BioS_831) to resolve seizures in a murine model using a previously established electroshock seizure assay.
Briefly, after dosing each mouse with either BioS_831, negative control (vehicle), or positive control (Sodium Valproate), electroshock
is delivered transauricularly using stimulation at 50 Hz and 50 mA for 0.8 seconds with a pulse width of 10 milliseconds. The total number
of hind limb flexes, hind limb extensions, and mortality rate is monitored for 60 seconds following electroshock, as are other adverse
events. We screened BioS_831 at both a low and high dose and found that at 40 mg/kg of BioS_831 significantly increased latency time to
tonic seizure induction and significantly reduced the number of observed tonic extension seizures, as compared to vehicle control. Notably,
unlike the ASM Sodium Valproate, BioS_831 did not cause sedation or ataxia. Sodium Valproate (VPA) while effective in this model at this
concentration, results in high levels of neurotoxicity, and has been associated with multi-organ failure, underscoring the importance
of not observing negative neurological effects with our novel compound. Post-study PK analysis showed good distribution of BioS_831 into
the brains of the test animals (average brain to plasma ratio 0.68). Since the electroshock seizure model is not based on seizure induction
through hypofunction of KCC2, these findings suggest that our zebrafish epilepsy primary screening model is capable of identifying novel
compounds that show translation to mammalian generalized epilepsy models and suggest that BioS_831 could further be optimized as a potential
anti-epileptic therapeutic.

Additionally, during the course
of this study we screened approximately 100 known neuroactives in our zebrafish model including clinical anticonvulsants, antidepressants,
antipsychotics, and dopaminergic signaling activators and inhibitors. The result is both an experimental platform and coupled computational
model that can identify both neurotherapeutics and neurotoxins, the