Acute Thrombolysis Reimagined

Basking is developing the first in class agent (BB-031) targeting von Willebrand Factor (VWF) along with a direct acting reversal agent (BB-025) to immediately the pharmacological effect of BB-031 in the event of bleeding. BB-031 is an RNA aptamer optimized for rapid onset of action and short duration of effect. Basking will initiate a Phase 2 trial in acute ischemic stroke in late 2022 and is exploring further application in pulmonary embolism in preclinical studies. The technology is based on two decades of translational research on RNA aptamers as therapeutic agents for cardiovascular diseases.

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 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 with reversal agent

BB-031 has demonstrated superiority to TPA across multiple murine and canine preclinical models while BB-025 expands the clinical utility allowing for hemostatic mod.

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 SOC allows:

  • Use in expanded time window
  • Expansion of eligible AIS patient population for acute revascularization
  • US addressable market: ~425k patients/year

Mechanism of Action

vWF drives both clot formation but also pathological expansion.

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


Reversible and Short Duration

  • Neutralization of drug effect in < 5 min if needed
  • ~3-hour pharmacodynamic effect
  • Well tolerated in GLP toxicology studies



Optimized for Stroke Therapy

  • Superior to rTPA in multiple animal models
  • Rapid onset of action (< 5 mins.)
  • BB-025 allows hemostatic modulation

Funding Update

Our recently closed Seed Financing supports development of BB-031 through Phase 1B, in parallel with the NIH funded BB-025’s IND enabling program.

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