Basking has successfully completed a Phase 1a single ascending dose safety study with BB-031 and is initiating a Phase 2 clinical proof-of-concept study in patients with acute ischemic stroke. The company is also conducting preclinical explorations of BB-031 in pulmonary embolism.
The company is developing BB-031, a first-in-class RNA aptamer targeting von Willebrand Factor (vWF), a critical, non-redundant driver of the clot formation, propagation and stabilization. In tandem, Basking is developing BB-025, a rapid-acting complementary oligonucleotide that immediately neutralizes BB-031 pharmacological activity in the event of bleeding. Preclinical research in multiple gold-standard animal models demonstrated that BB-031 quickly establishes recanalization of blocked blood vessels in the brain, as late as 6 hours after stroke onset.
Acute Stroke:
Deadly, Disabling, Undertreated
Current Treatment Pathway for Ischemic Stroke
Stroke is the second leading cause of death globally
- 1.7M annual cases in US, EU5, and Japan
- Adult global lifetime risk of as acute ischemic stroke (AIS) >18%
Current Treatments reach <15% of all Patients
- TPA associated bleeding risk limits utilization
- Clot accessibility and need for a surgeon limit usage of thrombectomy
Stroke is costly with poor outcomes
– Leading cause of long-term disability
~$240B annual US cost in 2030
Our Approach
Acute thrombolytic drug with a complementary reversal agent
BB-031 has demonstrated superiority to recombinant tissue plasminogen activator (rTPA) across multiple gold-standard experimental models. Reversal agent BB-025 expands the clinical utility of that agent by allowing for hemostatic modulation.
BB-031 Expands Eligible Patient Population for Stroke Therapy
Current Therapeutic Approaches
- rTPA: short therapeutic time window
- Endovascular mechanical thrombectomy: longer therapeutic time window but isn’t applicable to majority of patients
Basking Therapeutic Approach
Improved risk-benefit profile over standard-of-care (SOC) allows:
- Use in expanded time window
- Expansion of eligible as acute ischemic stroke (AIS) patient population for acute revascularization
- US addressable market: ~425k patients/year
Mechanism of Action
von Willebrand factor (vWF) drives both clot formation but also pathological expansion.
von Willebrand factor (VWF) influences thrombus initiation, amplification and propagation via multiple mechanisms
- Adhesion: Localize platelets to site of injury
- Aggregation: Binding platelets together via GpIb⍺-A1 axis
- Binds FVIII, amplifying secondary platelet activation
- Propagation: Self-associates, creating a long scaffold for platelet aggregation
- Inflammation: Recruits leukocytes, which catalyze inflammation
Safety
Reversible and Short Duration
- Neutralization of drug effect in < 5 min if needed
- ~3-hour pharmacodynamic effect
- Well tolerated in GLP toxicology studies
Efficacy
Optimized for Stroke Therapy
- Superior to rTPA in multiple animal models
- Rapid onset of action (< 5 mins.)
- BB-025 allows hemostatic modulation