| Total Companies | 6 |
|---|
| Phase 2 | 2 |
|---|
| Phase 1 | 2 |
|---|
| Preclinical/Discovery | 2 |
|---|
Kinase inhibitors represent a promising therapeutic approach for Alzheimer's disease, targeting key signaling pathways involved in protein aggregation, neuroinflammation, and neuronal survival. The main kinase targets include CDK5, GSK-3β, RIPK1/3 (necroptosis pathway), receptor tyrosine kinases, and related enzymes.
For detailed mechanism information, see Tau Kinase Inhibitors and CDK5 Inhibitors.
| Company |
Drug |
Target |
Status |
Development Notes |
| Inhibikase |
IkT-148009 |
c-Abl/RIPK1 |
Phase 2 |
Parkinson's, targets neuroinflammation via necroptosis |
| AB Science |
Masitinib |
KIT/PDGFR |
Phase 2/3 |
Mast cell modulation, neuroinflammation |
| Company |
Drug |
Target |
Status |
| Oligomerix |
OLX-07010 |
Tau oligomers/CDK5 |
Phase 1a |
| Alector |
AL044 |
TREM2 agonist |
Phase 1 |
| Company |
Program |
Target |
Stage |
| Vicore Pharma |
C21 |
AT2R + kinase signaling |
Phase 1 |
| Denali Therapeutics |
DNL151 (BIIB122) |
LRRK2 |
Phase 2b (PD) |
Program: IkT-148009 — c-Abl/RIPK1 kinase inhibitor
- Mechanism: Inhibits c-Abl tyrosine kinase and RIPK1-mediated necroptosis
- Status: Phase 2 enrolling for Parkinson's disease
- Relevance to AD: c-Abl activation contributes to tau pathology and neuronal death in AD
- Page: Inhibikase Therapeutics
Program: Masitinib — KIT/PDGFR inhibitor
- Mechanism: Tyrosine kinase inhibition targeting KIT and PDGFR
- Status: Phase 2/3 in Alzheimer's disease
- Relevance: Modulates mast cells and neuroinflammation; targets receptor tyrosine kinases
- Page: AB Science
Program: OLX-07010 — Tau self-association inhibitor
- Mechanism: Inhibits tau oligomer formation; modulates CDK5-mediated tau phosphorylation
- Status: Phase 1a clinical trials (first-in-human)
- Relevance to AD: Targets upstream of tau pathology; CDK5 is a key tau kinase
- Page: Oligomerix
Program: AL044 — TREM2 agonist
- Mechanism: TREM2 is a receptor tyrosine kinase-like immune receptor
- Status: Phase 1
- Relevance to AD: TREM2 signaling modulates microglial function; genetic variants confer AD risk
- Page: Alector
Program: C21 — AT2R (angiotensin II type 2 receptor) modulator
- Mechanism: AT2R has kinase-like signaling properties; C21 is an AT2R agonist
- Status: Phase 1
- Relevance to AD: AT2R signaling promotes neuroprotection and anti-inflammatory effects
- Page: Vicore Pharma
Program: DNL151 (BIIB122) — LRRK2 inhibitor
- Mechanism: LRRK2 kinase inhibition
- Status: Phase 2b LUMA trial in Parkinson's disease
- Relevance to AD: LRRK2 is expressed in microglia and may modulate neuroinflammation in AD
- Page: Denali Therapeutics
- Role: Phosphorylates tau at multiple sites, promoting aggregation
- Inhibitors in development: Oligomerix OLX-07010
- Page: CDK5
- Role: Major tau kinase; hyperphosphorylates tau in AD
- Inhibitors: Lithium, tideglusib (failed in clinical trials)
- Page: GSK-3β
- Role: Mediates necroptosis, a form of programmed cell death
- Inhibitors: Inhibikase IkT-148009
- Page: RIPK1
- Role: Modulate neuroinflammation, microglial activation
- Inhibitors: Masitinib (KIT/PDGFR), TREM2 agonists
- Page: TREM2
gantt
title AD Kinase Inhibitor Development Timeline
dateFormat YYYY
axisFormat %Y
section Phase 2/3
Masitinib (AB Science) :active, 2019, 2026
section Phase 2
IkT-148009 (Inhibikase) :active, 2024, 2027
section Phase 1
OLX-07010 (Oligomerix) :active, 2025, 2026
AL044 (Alector) :2025, 2026
C21 (Vicore) :2025, 2026
section Preclinical/Phase 2b (PD)
DNL151 (Denali) :2024, 2027