Pathogens mutate.
The host endures.
LuAnce New York is building a mitochondria-targeting therapeutic platform for the pathogens medicine cannot outrun. One molecule — Lu120819, powered by Luterion™ — advancing across pandemic influenza, carbapenem-resistant bacteria, filoviruses, and the ARDS–sepsis axis.
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Every pathogen-specific drug is one mutation from obsolete. We treat the part of the equation that doesn't change.
Mortality in severe infection is rarely a function of the pathogen alone — it is host mitochondrial failure, redox collapse, immune exhaustion, and systemic inflammatory injury. Lu120819 restores that machinery, and at high pathogen burden also disrupts the pathogen directly. The mechanism is indifferent to strain, serotype, and resistance genotype.
Efficacy independent of viral lineage or β-lactamase repertoire (KPC, NDM, OXA-48).
One CMC package, one tox package, one molecule — four indications on shared regulatory foundation.
Government stockpile procurement plus high-margin hospital critical-care channels.
Luterion™ — a mitochondria-targeting nanoparticle with a dual mechanism of action
A plant-derived, first-in-class particle. Lu120819 is the clinical embodiment: a universal shield for the host, and a targeted weapon at the pathogen interface.
The Universal Shield
Restores mitochondrial function, reverses T-cell exhaustion — lowering PD-1 on CD8+ T cells and recovering cytotoxic capacity — mitigates oxidative and ER stress, and stabilizes cellular energy supply — preventing the immune-metabolic collapse that drives mortality. Restores MAVS signaling suppressed by influenza NS1 and reinvigorates T-cell effector function via PD-1 downregulation.
The Physical Strike
At high pathogen burden, Lu120819 disintegrates viral envelopes and destabilizes bacterial outer membranes. There is no pathogen-specific target here — the particle acts on membrane architecture shared across Gram-negative and Gram-positive bacteria and fungi alike, which is why resistance status does not change the outcome and no β-lactamase pathway applies.
Measured against the bovine H5N1 isolate that defeated the standard of care — and against eleven bacterial and fungal strains
Two independent laboratories, two assay designs, two arms of the same mechanism. The host-directed arm is measured first — and the way it is measured is the reason the result matters.
The cell is treated first. Then the virus arrives.
OFF
Culture supernatant is drawn off and plaque-titred on fresh MDCK. Every plaque is one virion that successfully completed a full replication cycle. This is not a viability proxy, not CPE scoring, and not a binding assay — it is infectivity, in log₁₀ PFU/µL against the viral control.
Lu120819 is removed before H5N1 is introduced, so the inoculum is never neutralised in the tube and free particles cannot coat the incoming virus. Whatever suppresses replication is a change left behind in the cell. The falling titre is host-state, not chemistry in the medium.
A direct-acting antiviral that was washed off before infection should lose ground as replication compounds — its effect decays with dilution and time. This does the opposite. The pre-treated cell becomes progressively harder to replicate in, which is what a durable change to host state looks like: the mitochondrial and innate-immune reset is still holding a full day after the compound itself is gone.
6 points, threefold serial dilution, triplicate
viability curve flat across the full range — CC₅₀ never reached
The same particle clears eleven strains under dynamic contact
Korea Analysis Test Researcher
Duplicate, independent trials
Unlike the H5N1 work, this is direct-contact killing: Lu120819 at a final 3.3 × 10⁷ particles/mL was held with each organism in shaken suspension for 6 or 24 h, then plated for viable count. Eight of eleven strains were reduced 99.9 %, six of them below the 10 CFU/mL limit of detection — including Klebsiella pneumoniae, the species behind the CRE program, and MRSA.
Gram-negative and Gram-positive alike
Envelope-disrupting activity does not sort by cell-wall architecture: E. coli, K. pneumoniae and P. aeruginosa fall below detection alongside S. aureus and MRSA. C. albicans — a fungus — was reduced 99.9 % to 9.0 × 10¹ CFU/mL.
Resistance status is irrelevant
MRSA was reduced 99.9 % from 4.6 × 10⁷ CFU/mL to below detection — the same result as its drug-susceptible counterpart. A physical mechanism has no target for an efflux pump or a β-lactamase to defeat.
Two mechanisms, one particle
Direct contact kills bacteria at 10⁷ particles/mL. Host pre-treatment suppresses H5N1 at 10⁵ — two orders of magnitude lower, and after wash-off. The same particle is doing different work in each assay.
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Interrogate the
dual mechanism.
Now move the variables yourself. Set pathogen burden and the Lu120819 pre-treatment dose, then switch each arm of the mechanism on or off. Inhibition curves are anchored to the measured H5N1 infectivity IC₅₀; the amber curve is host-cell toxicity on uninfected MDCK, not efficacy.
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Curves fitted to measured IC₅₀ (infectivity, plaque titration of supernatant) and CC₅₀ (viability, uninfected MDCK) from report 03142025-CDJZ18 (Creative Diagnostics, Nov 2025). Compound applied as a 2 h pre-treatment and washed off before infection. In-vitro data — not predictive of human outcomes.
One molecule.
All programs advance Lu120819 (Luterion™) on a shared CMC, GLP-toxicology, and Phase 1 foundation. Select a program for detail.
EU-GMP nanoparticle manufacturing on a single process. Lu120819-200 supplied as a nebuliser solution for inhalation — the only route with a completed GLP toxicology package. IV and SC presentations are in development with our group affiliates.
Inhalation route only. Two-week repeat-dose inhalation toxicity in Han Wistar rats and Beagle dogs, run to GLP at Labcorp Drug Development. No adverse test-item–related findings in body weight, food consumption, haematology or clinical chemistry.
Cardiovascular NOAEL 75 mg/kg in conscious telemetered dogs — the highest dose tested. Respiratory and CNS NOAEL 46 mg/kg in rats; the mild CNS signs at 24 and 46 mg/kg were transient and fully resolved.
Ames bacterial reverse mutation, in-vitro micronucleus in human lymphocytes, and in-vivo rat bone-marrow micronucleus — all negative. No clastogenic or aneugenic potential.
Nonclinical dossier compiled against the inhalation protocol Lu120819-LA2025-INH-P1-1. Toxicokinetics show low systemic accumulation. First-in-human ready pending indication selection.
Pandemic Influenza — H5N1
Lu120819 · discovery · most advanced dataset · government stockpile
INH / IV*
~50% case fatality in confirmed human cases. Oseltamivir showed no therapeutic effect against the U.S. human-derived TX/37 (D1) isolate; polymerase inhibitors required exposures far above safe human dosing (Nature 636, 711–718, 2024).
Discovery stage. Independent in-vitro testing against the bovine H5N1 Texas/2024 isolate: IC₅₀ 6.95 × 10⁵ particles/mL at 24 h and 1.17 × 10⁵ at 48 h (R² 0.984 / 0.947), with MDCK CC₅₀ > 1.22 × 10⁸ — a selectivity index above 1,000×. No in vivo challenge study has been run in this indication. Lethal-challenge efficacy in ferret or mouse models is the next gate.
U.S. procurement potential $750M–$1.5B; global $2.5B+; five-year addressable market ~$4.0B. BARDA / ASPR pandemic-track engagement from 2027.
Carbapenem-Resistant Enterobacterales
Lu120819 · discovery · CRE bloodstream infection · hospital channel
IV*
WHO priority #1 pathogen class. Multi-enzyme resistance (KPC, NDM, OXA-48) defeats existing antibiotics; salvage regimens carry severe toxicity and rising failure rates.
Mechanism-novel bactericidal action via ROS imbalance and ATP collapse, combined with restored phagocyte metabolism — no reliance on traditional antibiotic targets.
Discovery stage. In dynamic-contact testing (modified ASTM E 2149), K. pneumoniae fell from 8.4 × 10⁶ CFU/mL to below the 10 CFU/mL detection floor — 99.9 % reduction at 3.3 × 10⁷ particles/mL. MRSA and P. aeruginosa matched it. No animal infection model has been run. High-margin specialty commercial sales into tertiary hospital systems once in vivo proof-of-concept and an indication-specific development plan are in place.
Filovirus — Ebola & Marburg
Lu120819 · discovery · new 2026 program · biodefense
INH / IV*
Outbreak case fatality of 25–90%. Licensed monoclonals and vaccines cover Zaire ebolavirus only — Sudan virus and Marburg have no approved therapeutic or vaccine.
Filoviral death is driven by host pathology — cytokine storm, endothelial and coagulopathic failure, mitochondrial exhaustion. A species-agnostic host-resilience agent covers the entire family, including divergent strains, and enveloped filovirions are susceptible to direct disruption.
Discovery stage — no filovirus data generated to date. BSL-4 collaboration in negotiation for pseudotyped and authentic-virus screening; Animal Rule development path scoped with federal biodefense partners.
ARDS–Sepsis Axis
Lu120819 · discovery · new 2026 program · infection-driven critical care
IV*
Sepsis accounts for roughly 11 million deaths annually; ICU mortality in moderate-to-severe ARDS remains near 40%. There is no approved pharmacotherapy for either — care is supportive only.
ARDS and sepsis are the terminal common pathway of severe infection — precisely the immune-metabolic collapse Lu120819 was designed to reverse. Restoring mitochondrial ATP metabolism protects alveolar-capillary integrity, restores phagocytic capacity, and mitigates sepsis-induced organ injury independent of the causative organism.
The largest addressable population in the portfolio and the clearest bridge from biodefense contracts to everyday hospital revenue. Discovery stage — translational package in build; a CLP or caecal-ligation in vivo readout is the next gate.
Four indications, scored on the axes that decide capital allocation
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The nexus of biodefense, clinical science, and global capital
Announcement
Joining Alexandria LaunchLabs® at the Alexandria Center® for Life Science
LuAnce New York begins residency September 1, 2026 — placing our laboratory operations inside Manhattan's life-science core, minutes from the hospital systems and BSL-3 capacity our programs depend on.
Clinical epicenter
Direct access to Mount Sinai, Columbia, Cornell, NYU and MSK — and to high-burden CRE and critical-care populations for rapid trial execution.
Biodefense & policy hub
Proximity to BARDA, ASPR, NIH and UN global-health bodies accelerates contracting, regulatory pathways, and policy adoption.
Capital & talent magnet
The world's deepest pool of institutional capital, strategic pharma partners, and clinical-operations talent.
A capital-efficient path
to clinical validation
The platform package is closed — see readiness in 05. What follows is the sequence that turns it into clinical evidence, one gate at a time.
NYC operations
Residency at Alexandria LaunchLabs from September 1. First in vivo efficacy studies initiated — the gate every indication currently sits behind.
Phase 1 foundation
SAD/MAD study establishing safety, PK/PD, and dose justification across all four indications, running in parallel with in vivo proof-of-concept work.
Proof of concept
Contingent on in vivo readouts: Phase 2 in CRE bloodstream infection and ARDS–sepsis; BARDA engagement on the H5N1 and filovirus pandemic tracks.
Pivotal & submission
Pivotal trials, Emergency Use Authorization for pandemic indications, and BLA submission for CRE.
Discovery, translation, and regulatory strategy in the same room
Jaekyung Cecilia Song, JD, PhD
Leads LuAnce’s scientific strategy, translational development, regulatory planning, and global partnering. Her background spans biomedical science, therapeutic development, legal strategy, and international collaboration.
- ·BS in Biology, Massachusetts Institute of Technology
- ·PhD in Molecular Physiology, University of Cincinnati College of Medicine
- ·MS in Medical Sciences, Boston University School of Medicine
- ·JD, Seoul National University School of Law
- ·Former research laboratory leadership, Beth Israel Deaconess Medical Center / Harvard Medical School
- ·Former endowed-chair professor, Dankook University
Woncheol Mikael Choi, KMD, PhD
Founder of the Luterion group and the discoverer of Luterion™, the mitochondria-derived nanoparticle platform underpinning the group’s host-directed research. He brings decades of integrative oncology practice, translational research, and an extensive global patent portfolio.
- ·BS & MS in Korean Medicine; PhD in Pharmaceutical Sciences and PhD in Korean Medical Science
- ·Academician & Foreign Member, Russian Academy of Sciences
- ·Founder & CEO, Luterion Co., Ltd.
- ·Former Professor of Oncology, Kyung Hee University College of Korean Medicine
- ·Former Endowed-Chair Professor and Vice Chancellor, Dankook University
- ·Inventor on an extensive portfolio of granted international patents
LuAnce New York, Inc.
New York City
Alexandria LaunchLabs® at the Alexandria Center® for Life Science from September 1, 2026.
- Government & biodefense partners (BARDA, ASPR)
- Academic and BSL-3 / BSL-4 collaborators
- Institutional and strategic investors
© 2026 LuAnce New York, Inc.
Luterion™ · Lu120819
Forward-looking statements — for informational use only