Depleting the cell at the center of the disease.
Calixis is developing an oral small molecule that inhibit wild-type KIT — the receptor mast cells depend on to survive. Here is how the approach works, what we are studying, and where we are headed.
The KIT survival signal — and how we switch it off
Mast cells rely on a receptor called KIT. When its natural partner, stem cell factor (SCF), binds KIT, the receptor sends a signal that keeps the mast cell alive. Block that signal, and mast cells can no longer survive.
Bind
Our small molecule enters the mast cell and occupies KIT's kinase site, where the receptor normally relays its signal.
Block
With the kinase silenced, SCF can no longer tell the mast cell to survive and multiply — even when SCF is present.
Deplete
Deprived of their survival signal, mast cells decline in number, reducing the source of the mediators that drive disease.
A different target than cancer KIT inhibitors
You may have heard of KIT inhibitors in oncology. Those are built to hit mutated KIT that drives certain tumors.
Calixis focuses on wild-type KIT — the normal, unmutated receptor found on healthy mast cells. Our goal is to modulate normal mast-cell biology in allergic and inflammatory disease, a fundamentally different objective, with selectivity designed for that setting.
- Wild-type selective
- Oral small molecule
- Designed for chronic use
- Non-oncology
From a single cell to a chronic disease
Chronic spontaneous urticaria (CSU) is defined by recurring hives and swelling that appear without an obvious trigger for six weeks or more. Mast cells are central to this process.
1 · Mast cells accumulate
Mast cells reside in the skin, maintained by KIT signaling, ready to respond to stimuli.
2 · They degranulate
The cells release histamine and other mediators into surrounding skin tissue.
3 · Symptoms appear
Mediators cause the wheals, swelling, and intense itch that define the disease — often for years.
Because mast cells are upstream of the many mediators involved, reducing the cells themselves is a strategy to address the disease closer to its source.
Where our programs stand
Our lead program is in Phase 2 in chronic spontaneous urticaria, with additional mast-cell–driven indications planned.
| Program | Target | Indication | Stage | Status |
|---|---|---|---|---|
| THB335 Oral · lead candidate |
Wild-type KIT | Chronic spontaneous urticaria |
DiscoveryINDPh 1Ph 2Ph 3
|
Phase 2 · ongoing |
| THB335 Oral · lifecycle |
Wild-type KIT | Additional mast-cell driven diseases |
DiscoveryINDPh 1Ph 2Ph 3
|
Planning |
| THB3093 Oral · pipeline |
Wild-type KIT | Mast-cell–driven diseases |
DiscoveryINDPh 1Ph 2Ph 3
|
Lead Nominated |
Built to reach many diseases
Chronic spontaneous urticaria is a clear, mast-cell–driven starting point. But the same biology recurs across allergy, dermatology, and beyond. Our long-term vision is a portfolio of therapies that share one core idea — that carefully depleting mast cells can relieve disease at its source. Each new indication is chosen where the evidence for mast-cell involvement is strong.
- Chronic urticaria
- Allergic disease
- Mast cell disorders
- Atopic conditions
- Respiratory
Want to go deeper on the science?
We're happy to share more with investigators, partners, and investors.
Contact our team