Breathes With Your Lungs
Listen to the Science
Explore the breakthrough science of mechanopharmacology and breathing nanoparticles in our latest episode.
Breathing Nanoparticles & Mechanopharmacology
S-BAL Science Series
Discover how S-BAL's mechanosensitive nanoparticles respond to the physical forces of breathing, delivering therapeutic payloads precisely when and where they're needed. This episode explores the cutting-edge science behind our biomimetic approach to treating respiratory diseases.
The Challenge of a
Single Breath
For most of us, breathing is unconscious. But for a premature infant or a patient with severe lung injury, every single breath is a monumental struggle.
Healthy Alveolus
Natural surfactant coats the alveoli, reducing surface tension to near-zero during exhalation, preventing collapse.
Surfactant Deficiency
Without functional surfactant proteins SP-B and SP-C, surface tension remains high, causing alveoli to collapse with each breath.
Understanding Surfactant Protein Deficiencies
The core pathophysiology: Mutations in SFTPB, SFTPC, and ABCA3 genes disrupt surfactant protein synthesis, causing severe respiratory distress syndrome. Lung transplantation remains the only definitive treatment—until now.
Why Current Surfactant Therapy
Fails on Four Fronts
While surfactant replacement therapy has reduced neonatal mortality from >50% to <10%, it remains fundamentally flawed for genetic surfactant deficiencies.
Static Functionality
Cannot adapt to breathing dynamics
Current therapies are passive agents incapable of responding to the dynamic mechanical forces of respiration. Natural surfactant continuously adapts its molecular organization—static replacements cannot replicate this.
Distribution Heterogeneity
Non-uniform alveolar coverage
Intratracheal bolus administration results in gravitational pooling and preferential flow to already-open lung units, leaving collapsed regions untreated.
Biochemical Vulnerability
Rapidly inactivated by serum proteins
Plasma proteins like albumin and fibrinogen leak into alveoli during lung injury and competitively adsorb to the air-liquid interface, raising surface tension to pathological levels.
Temporal Limitations
Only 24-48 hours of function
Functional duration is severely limited, necessitating frequent invasive re-administration with cumulative risks of infection, pneumothorax, and ventilator-associated complications.
The Unmet Need
For patients with genetic surfactant deficiencies, these limitations translate to hundreds of invasive interventions before definitive treatment via lung transplantation. Current therapies provide temporary relief but cannot address the underlying need for dynamic, adaptive surface tension regulation that mirrors healthy lung function.
A Revolutionary Mechanopharmacological Approach
S-BAL is the first therapeutic platform to replicate the dynamic, adaptive behaviour of healthy pulmonary surfactant. It is not just a replacement; it is an autonomous, intelligent system.
Closed-Loop
Breathing Response
Inhalation
Alveolar Stretch
Lungs expand, creating 8-12% biaxial strain
S-BAL Activates
Mechanosensitive Response
Nanoparticle opens in 186ms
Surfactant Released
Surface Tension Drops
Achieves 2.8 mN/m minimum
Exhalation
S-BAL Deactivates
Returns to protected closed state
Closed-Loop Breathing Response System
Inhalation
Alveolar Stretch
Lungs expand, creating 8-12% biaxial strain
S-BAL Activates
Mechanosensitive Response
Nanoparticle opens in 186ms
Surfactant Released
Surface Tension Drops
Achieves 2.8 mN/m minimum
Exhalation
S-BAL Deactivates
Returns to protected closed state
"Mechanopharmacology" — The use of mechanical stimuli to control the activity of a therapeutic agent.
How MSP-28 Peptides Work
The mechanosensitive peptide MSP-28 is the core innovation enabling S-BAL's autonomous response to breathing mechanics.
Conformational States
Response Time
0 ms
Transition occurs faster than a single breath cycle
Activation Threshold
8-12%
Biaxial strain matching natural alveolar expansion
Reversibility
0%
Fully reversible conformational change
Cycle Stability
0+
Maintains function across thousands of breathing cycles
Precision-Engineered for Autonomous Therapy
PLGA Polymer Core
Biodegradable structural foundation providing controlled clearance over 7-30 days.
Lipid Shell
Biomimetic phospholipid mixture (DPPC:PG:DOPE:Chol:DSPE-PEG2000) mimicking natural surfactant composition.
PEG Stealth Corona
Provides immune evasion by reducing opsonisation, prolongs residence time, and ensures biocompatibility.
MSP-28 Mechanosensitive Peptides
The 'sensor.' Embedded peptides that adopt a kinked helical state and trigger payload release upon mechanical strain.
SP-B & SP-C Protein Analogues
The 'payload.' Encapsulated synthetic proteins that restore the critical function of natural surfactant.
A New Era of Therapy
Actively Responds to Every Breath
Unlike static therapies, S-BAL nanoparticles sense alveolar stretch and release their therapeutic payload on demand. The mechanosensitive peptides (MSP-28) trigger a helix-to-coil transition in just 186 milliseconds, perfectly synchronized with natural breathing.
52% Better Than Natural Surfactant
S-BAL achieves a minimum surface tension of 2.8 mN/m—significantly exceeding the clinical target of 5 mN/m. Natural surfactant only reaches 5.8 mN/m under the same conditions.
Lasting 7-10 Days, Not Hours
By remaining in a protected 'closed' state until activated, S-BAL shields its payload from the lung's harsh environment. It maintains over 75% functional activity for 7-10 days—transforming treatment from daily to weekly administration.
Thrives in Diseased Lung Environments
In the presence of 10% serum proteins that typically disable conventional therapies, S-BAL maintains 92% functionality. Conventional preparations drop to just 35% under identical conditions.
Actively Promotes Lung Regeneration
Beyond mechanical function, S-BAL demonstrates remarkable regenerative properties: 242% improvement in lung organoid growth, 358% increase in progenitor cell colonies, 78% reduction in inflammatory TNF-α, and over 500% boost in anti-inflammatory IL-10.
Exceptional Biocompatibility Profile
Cytotoxicity
>91% Cell Viability
Across three pulmonary cell lines (A549, BEAS-2B, Primary AEC II) at concentrations up to 1000 µg/mL.
Hemocompatibility
<1.8% Hemolysis
Well below the 2% biomedical acceptability threshold. No platelet activation or coagulation interference observed.
Immunogenicity
Minimal Response
No significant cytokine release (TNF-α, IL-6). Minimal complement activation. No anti-drug antibodies detected.
Biodegradation
Complete Clearance
PLGA core degrades via first-order kinetics with full clearance by day 30. Lipid components integrate into endogenous pools.
Beyond Replacement: Active Regeneration
S-BAL doesn't just restore surfactant function—it actively promotes lung tissue repair and reduces inflammation.
Improvement in lung organoid development and maturation
Increase in lung progenitor cell colony formation
Decrease in pro-inflammatory cytokine levels
Increase in anti-inflammatory cytokine production
Multi-Faceted Therapeutic Platform
S-BAL represents a paradigm shift: from passive surfactant replacement to an active, regenerative therapy that addresses the underlying tissue damage in respiratory diseases.
Transforming Treatment Across Multiple Indications
S-BAL's mechanopharmacological platform offers therapeutic potential across a spectrum of respiratory conditions.
Neonatal RDS
Primary indication for premature infants with underdeveloped surfactant systems
15M babies born preterm annually
ARDS
Acute respiratory distress syndrome in critically ill adults
3M cases globally per year
COPD
Chronic obstructive pulmonary disease with surfactant dysfunction
380M patients worldwide
IPF
Idiopathic pulmonary fibrosis with progressive lung scarring
5M patients globally
COVID-19 Lung Injury
Post-viral surfactant dysfunction and lung damage
Millions affected by long COVID
Lung Transplant
Surfactant support for transplanted lungs and donor preservation
4,500+ transplants/year
Join the S-BAL Development Journey
We are actively seeking partners to accelerate the clinical translation of S-BAL. Whether you are a research institution, clinical facility, or pharmaceutical partner, we invite you to be part of this groundbreaking advancement in respiratory medicine.
Clinical Trial Sites
We are seeking qualified clinical facilities with expertise in neonatal intensive care, pulmonology, or respiratory medicine to participate in our upcoming Phase II trials.
- NICU and PICU facilities
- Academic medical centers
- Specialized respiratory units
Research & Development Partners
We welcome collaborations with research institutions and pharmaceutical companies interested in co-developing or licensing our mechanopharmacology platform.
- Joint development agreements
- Technology licensing opportunities
- Strategic partnerships
Interested in Partnering for Phase II?
Contact our partnership team to discuss collaboration opportunities.
A Clear Path to Clinical Translation
Foundational Science
- Comprehensive in-vitro proof-of-concept
- Mechanism of action elucidated
- Lead formulation optimised
- Scalable manufacturing process developed
Preclinical Development
- IND-enabling toxicology and safety studies
- Efficacy validation in large animal models of ARDS
- GMP manufacturing scale-up and batch release
Clinical Development
- Phase I First-in-Human trial in ARDS patients (safety, PK/PD)
- Phase II trials in target indications (Neonatal RDS, genetic deficiencies)
- Seek Orphan Drug and Fast Track designations
Partnership & Commercialisation
- Engage strategic partners for late-stage development
- Commercial launch preparation
- Global market access strategy
Intellectual Property: 3 provisional patents filed covering core technology, composition, and manufacturing.
Regulatory Milestones
Administration
S-BAL has been registered with the FDA Office of Orphan Products Development (OOPD) programs, positioning us for expedited regulatory pathways including Orphan Drug Designation, Fast Track status, and potential Breakthrough Therapy designation for genetic surfactant deficiencies. Our manufacturing process uses microfluidic nanoprecipitation with a Quality by Design (QbD) approach to maintain high quality while reducing costs.
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