Cornerstone Clinical Asset · Non-Oncology Fields Only

SAPU003. IV nano-everolimus for pediatric neurology and healthy aging.

Clinical-stage. GMP manufactured. Human safety data in hand. ODD, RPDD, and Priority Review Voucher are the planned regulatory levers — none filed or granted yet. Licensed from Sapu Biosciences into PDAOAI — neurology and longevity fields only. Sapu retains worldwide oncology.

Indications — Non-Oncology Only

Pediatric neurology + healthy aging.

PDAOAI's SAPU003 franchise covers two fields only: rare pediatric neurology (mTORopathies) and healthy aging / longevity. Oncology remains with Sapu Biosciences worldwide. Prevalence across these indications: ~72,000 US, roughly 140,000 across US + EU5 — prevalence, not the treated or reimbursed population, and not additive across rows.

IndicationTierIncidence / PrevalencePatients (US)
Tuberous Sclerosis Complex (TSC)Tier 1~1:6,000–1:10,000 live births~50,000
Focal Cortical Dysplasia (FCD)Tier 1~1:25,000 prevalence~14,000
GATOR1-related epilepsy (DEPDC5, NPRL2, NPRL3)Tier 2~1:35,000–1:50,000 live births~5,000–9,000 (est.)
MTOR gain-of-function syndromes (germline; Smith-Kingsmore)Tier 2~1:32,000,000<100 diagnosed

Population incidence or prevalence — not treated or reimbursed patients. Rows overlap biologically (somatic MTOR and DEPDC5 variants drive much of FCD type II) and are not additive. Sources: GeneReviews 2024 and TSC Alliance (TSC); López-Rivera et al. 2022 (FCD; surgically treatable lesions); Symonds et al. 2019 (GATOR1; US count derived); Raski & Prada 2026 (Smith-Kingsmore).

Adjacent — longevity and healthy aging. Same intermittent-IV mTOR modulation profile applies to healthspan biomarker programs. In-scope for PDAOAI alongside neurology.
Mechanism

Root pathway → downstream circuit → therapy.

The biology holds together at three levels: mTOR as the root, KCC2 as the downstream chloride cotransporter, and GABAergic signaling as the clinical readout.

Step 1

Root pathway

mTOR pathway dysregulation drives multiple pediatric epilepsy syndromes across the mTORopathy spectrum. Both mTORC1 and mTORC2 signaling implicated.

Step 2

Downstream circuit

mTOR hyperactivation impairs KCC2, the neuronal chloride cotransporter. Chloride accumulates inside neurons. GABA — the brain's main inhibitory signal — flips from calming to excitatory. Neurons fire uncontrolled. Seizures.

Step 3

Therapeutic action

SAPU003 is designed to act on this chain: inhibit mTOR → restore KCC2 function → normalize chloride homeostasis → GABA regains its inhibitory role → seizures suppressed. The chain has been demonstrated with rapamycin in a preclinical model, not yet with SAPU003 — confirming it for SAPU003 is Workstream III. Reference: Bakouh N, et al. Brain 2025;148(2):549–563.

Differentiation

Why SAPU003, not oral everolimus (Afinitor).

Oral everolimus is FDA-approved and works — for the indications where oral delivery is sufficient. SAPU003 is the intravenous nanoparticle reformulation that changes the pharmacokinetics.

FeatureSAPU003 (IV nanoparticle)Oral rapalogs (Afinitor)
RouteIntravenousOral
GI absorptionBypassedVariable
First-pass metabolismBypassedSignificant
Food effectNoneYes
Onset / exposureRapidSlower / variable
Drug interactionsReducedHigh (CYP3A / P-gp)
Dosing paradigmIntermittentContinuous daily
Chronic GI exposureMinimizedPersistent
Microbiome impactLower riskHigher risk
Preclinical PK. ~90× higher Cmax and ~13× higher AUC vs. oral everolimus. The program is designed around rapid CNS engagement for refractory and acute seizure settings that oral rapalogs cannot reach fast enough. Everolimus is a P-gp substrate, so CNS exposure is measured, not assumed — penetration studies sit in Workstream IV.
Supporting Science

Published foundations.

The formulation and the delivery class behind SAPU003, in the peer-reviewed record.

Int J Mol Sci · 2026

Intravenous Everolimus Formulation (Sapu003) for Clinical Trials

Min SH, Forero K, Putnam W, Anderson J, Hoff R, Lopp J, Trieu V, Ho K, Lee C.
Int J Mol Sci. 2026;27(13):5775

Formulation discovery, cGMP manufacturing and physicochemical characterisation of SAPU003.

doi:10.3390/ijms27135775 →

Int J Mol Sci · 2025

Sub-15 nm Nanoparticles for Drug Delivery: Emerging Frontiers and Therapeutic Potential

De T, Trieu V, Myers S, Qazi S, Saund S, Lee C.
Int J Mol Sci. 2025;26:10842

The sub-15 nm delivery class SAPU003 sits in.

doi:10.3390/ijms262210842 →

Planned Regulatory Pathway

Orphan + rare pediatric → Priority Review Voucher.

None of these designations have been filed or granted yet. This is the pathway the IND-enabling program is targeting — the three regulatory levers that make a small-population pediatric neurology asset economically meaningful.

ODD · Planned

Orphan Drug Designation

Target: file ODD applications for Tier 1 mTORopathies (TSC, FCD) once IND-enabling data supports it. If granted, ODD carries 7-year U.S. market exclusivity, tax credits, and development incentives for the qualifying rare indication.

RPDD · Planned

Rare Pediatric Disease Designation

Target: file Rare Pediatric Disease Designation to qualify for a Priority Review Voucher on approval. Recent Priority Review Vouchers have sold at $150–200M (Jazz Pharmaceuticals: $200M, Jan 2026). Program reauthorized through September 2029. Optionality only — not booked value.

Accelerated · Available

Accelerated approval paths

Pediatric exclusivity extension (6 months) and Breakthrough / Accelerated Approval pathways are available for high-unmet-need pediatric neurology. Eligibility to be established on the biomarker package generated in the IND-enabling program.

Development Plan

Four workstreams. 12–18 months to neurology IND.

The IND-enabling program is organized to accelerate biomarker data on existing clinical patients while running parallel translational and regulatory work.

I

Biomarker Acceleration

Timeline: Immediate. Collection and analysis on existing clinical SAPU003 patients — PBMCs, plasma, exosomes, cfDNA, cytokine panels. Every patient generates biomarker data that would otherwise take years and millions in a separate program.

II

Regulatory & Rare Disease Strategy

Timeline: 6–12 months. ODD and RPDD applications for Tier 1 mTORopathies (TSC, FCD). Natural history review. Regulatory briefing package. Development roadmap.

III

KCC2–mTOR Translational Validation

Timeline: 6–18 months. Focused preclinical studies on three questions: does SAPU003 restore KCC2 function; does it normalize chloride homeostasis; can KCC2 serve as a predictive biomarker for patient selection.

IV

CNS Exposure & Intermittent Dosing

Timeline: 6–12 months. PK modeling, CNS penetration studies, exposure-response modeling. Establishes SAPU003's primary differentiation vs. oral rapalogs quantitatively.

Deal Structure

Field-limited license from Sapu Biosciences.

Sapu Biosciences Retains

Asset ownership + oncology worldwide

Compound IP, the Deciparticle™ nanoparticle platform, and worldwide oncology rights.

PDAOAI Holds

Exclusive neurology + longevity, worldwide

Exclusive worldwide development and commercial rights across the neurology and longevity fields. Structured on standard field-license economics.

Right of reference to the clinical data.

PDAOAI holds right of reference to Sapu's clinical safety and pharmacokinetic data for SAPU003. The formulation has been dosed in humans and that record is available to the neurology program — so the IND package starts from real human exposure to this nanoparticle, not from the oral active alone.

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