Targeted protein degradation · 2026
End organ damage is an inflammatory event.
Moktra Bio builds protein degraders against scaffold kinases in inflammation. Lead program: MKT-001, in development for cardiac surgery–associated acute kidney injury.
Selected & supported by
Nucleate Bay Area Activator
Bakar Labs · CABL Awardee
Nucleate Demo Day · Genentech Forum
The approach
The biology was right. The modality was wrong.
Anti-inflammatory drugs have failed for thirty years across more than forty clinical programs and $5B+ of R&D. The targets weren’t the problem.
In a small clade of kinases within the TKL family, the protein scaffold, not the catalytic activity, is what drives end-organ inflammation. Inhibitors block the kinase domain and the scaffold survives. Degraders remove the protein entirely.
Moktra Bio builds heterobifunctional protein degraders against this clade, with the lead program in cardiac surgery–associated acute kidney injury.
Failed era
40+
Clinical programs against this biology in the inhibitor era.
Capital deployed
$5B+
In R&D against scaffold-kinase biology, zero approvals.
Approved Rx
0
FDA-approved preventive therapies for the lead indication today.
The platform
Our discovery engine compounds chemistry across the TKL clade.
Each Moktra program inherits from clinical-stage scaffold-kinase degraders and published chemistries in the TKL clade. Warhead chemotypes, linker geometry rules, and E3 cooperativity patterns all transfer between programs.
We walk to the nearest unaddressed neighbor in the clade. The clade-restricted starting point collapses chemical search space by roughly 8× before the first compound is synthesised.
Each program compounds learnings into the next. Cooperativity, selectivity, and linker SAR transfer forward; cost per program drops 2–3× across the platform.
13.5K → 1.6K
Search space, full kinome → TKL clade
The pipeline
One program in the clinic-readiness phase. Four more in the clade.
Program
Target
Indication
Modality
Stage
MKT-001
UndisclosedTKL scaffold kinase
CSA-AKICardiac surgery–associated AKI
VHL-recruiting PROTACCRBN backup · IV, pre-op
Discovery · Hit ID
MKT-002
TKL cladetarget undisclosed
End-organ injuryto be announced
Heterobifunctionalclade chassis
Target nomination
MKT-001
Lead program
MKT-001 is a heterobifunctional protein degrader that recruits the VHL E3 ligase to an undisclosed TKL-clade scaffold kinase, eliminating a scaffold function that drives inflammatory cell death in injured tissue. A CRBN-recruiting backup chemotype is in parallel.
The asset is designed for a single intravenous dose administered at the start of cardiac surgery — a scheduled, controlled window that bypasses the chronic PK and oral bioavailability constraints typical of degrader programs.
Cardiac surgery–associated AKI affects 30–40% of patients undergoing cardiac surgery. No FDA-approved preventive therapy exists today. A successful clinical readout enables the first 505(b)(1) NCE in this indication with Fast Track plausibility.
The team
Kartik Gupta, PhD
Founder & CEO
UW–Madison — scaffold-kinase pathway biology in inflammatory cell death. Merck postdoc. Industry PROTAC scientist.
Build with usSAB and chemistry advisory in formation · IP counsel: Fenwick & West · Moktra Bio Inc., Delaware C-corp.