.png)
SCIENCE & INNOVATION
Next-generation targeted therapies
At Kairos, we are establishing new treatment paradigms by designing small molecule therapeutics with novel mechanisms of action and exceptional selectivity - addressing unmet medical needs and improving the lives of patients with limited treatment options.
OUR APPROACH
Developing a proprietary pipeline
Our discovery platform combines cutting-edge medicinal chemistry, structural biology, and optimization guided by pharmacokinetic and pharmacodynamic principles to generate highly selective small molecule therapeutics.
These candidates are evaluated in disease-relevant cancer models to elucidate their mechanism of action and guide indication strategy - accelerating the development of targeted therapies with meaningful clinical impact.
These candidates are evaluated in disease-relevant cancer models to elucidate their mechanism of action and guide indication strategy - accelerating the development of targeted therapies with meaningful clinical impact.
Program
Indications
Discovery
Preclinical
Phase I/II/III
KDX350
Bivalent CK2ɑ Inhibitor
Solid tumors (including renal & colorectal carcinoma)
KDXXX
CDK degraders
Undisclosed
OUR LEAD ASSET
A new chapter in CK2 targeting : bivalent precision, deep tumor impact
CK2 is a master regulator of survival and resistance pathways across a wide range of cancers - including pediatric and orphan indications. Its clinical relevance is well supported by decades of research.
With our lead asset, we are advancing a bivalent small molecule inhibitor that engages both the ATP-binding pocket and a neighboring allosteric site on the CK2α subunit. This dual-site binding enhances selectivity, sustains inhibition, and blocks both catalytic activity and non-catalytic pro-survival functions of CK2.
Unlike first-generation CK2 inhibitors, our approach was specifically designed to overcome historical limitations - driving selective cancer cell death through a differentiated, validated mechanism with the potential for durable clinical impact.
With our lead asset, we are advancing a bivalent small molecule inhibitor that engages both the ATP-binding pocket and a neighboring allosteric site on the CK2α subunit. This dual-site binding enhances selectivity, sustains inhibition, and blocks both catalytic activity and non-catalytic pro-survival functions of CK2.
Unlike first-generation CK2 inhibitors, our approach was specifically designed to overcome historical limitations - driving selective cancer cell death through a differentiated, validated mechanism with the potential for durable clinical impact.
.webp)
Selectivity
Our bivalent inhibitor engages a cryptic allosteric pocket conserved within CK2 but divergent across the broader kinome - enabling high selectivity and reduced off-target effects.
Cancer persistence
Our bivalent binding strategy enables prolonged CK2 engagement and functional blockade, aiming to disrupt mechanisms of tumor adaptability and persistence - key contributors to relapse in difficult-to-treat cancers.
Broader functional modulation
Beyond catalytic inhibition, allosteric site engagement may interfere with CK2’s pro-survival functions that are not addressed by classical ATP-competitive inhibitors - offering a broader therapeutic effect.
Tumor-selective cell death
Unlike pan-kinase inhibitors, our compound has demonstrated preferential cytotoxicity in tumor cells over healthy cells in preclinical models - supporting the potential for reduced systemic toxicity and broader therapeutic windows.
Meet our Team
APPLICATION
Substantial opportunity in targeted oncology
CK2 is broadly overexpressed in tumors with high unmet need. Our preclinical data show potent anti-tumor activity across diverse models - both as monotherapy and in combination with standard-of-care - validating CK2 inhibition across genetically distinct patient populations.
Renal Cell Carcinoma
Total incidence
~108,000
US and EU5
~108,000
US and EU5
Colorectal cancer
Total incidence
~400,000
US and EU5
~400,000
US and EU5
Additional tumor types
We are actively exploring the potential of our bivalent CK2 inhibitor across additional tumor types where CK2 is overexpressed or plays a critical role in disease progression.
WHAT’S NEXT
Key achievements & Roadmap Milestones
2022
Scientific inception & Recognition
Founded in late 2022.
- Awarded French Tech Seed label, preclinical proof-of-concept through incubation within Pulsalys
- Winner of i-PhD, i-Lab, and Tech Tour 2022 innovation awards.
- Raised €1.5M pre-seed from business angels, family offices, and grants.
2023
Validating our vision
- CLARA Proof-of-Concept for bivalent CK2ɑ inhibitor
- MATWIN "Quick Pitch" Award, selected by a jury composed of MATWIN Board members and the full MEET2WIN audience
2024
Advancing toward the clinic
- Bpifrance €1.5M grant secured for preclinical-to-regulatory transition of first solid tumor candidate.
- First peer-reviewed data published in iScience
- Lead optimization achieved for bivalent CK2 inhibitor
2025-2027
SEED Round & Clinical Translation
- Advancing regulatory development of bivalent CK2 inhibitor, including CMC, safety, and toxicology studies.
- Clinical strategy implementation, with biomarker-guided expansion across multiple solid tumor types.
2028-2030
Pre-Series A & First-in-Human Milestones
- IND-enabling package completion and First-in-Human safety study initiation.
- Dose expansion cohorts planned in renal cell carcinoma, colorectal cancer, and other selected solid tumors
.png)