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How does Alectinib, a kinase inhibitor, achieve high-affinity binding to complement protein C1q?

PARTIALLY ADDRESSED

The abstract reports that Alectinib binds C1q with high affinity, but this is mechanistically unexpected since Alectinib is designed as a kinase inhibitor while C1q is a complement protein. Understanding this binding mechanism could reveal new drug-target interaction principles and inform rational design of complement modulators. Gap type: unexplained_observation Source paper: Complement C1q-Targeted Microglial Membrane Camouflaged Nanolipid Carriers for Synaptic Protection in Alzheimer's Disease: A Bioinspired Alectinib Delivery Strategy. (2026, Nano letters, PMID:41114949)

Priority: 0.87 Domain: neuroinflammation Hypotheses: 0
📊 Landscape Analysis

Landscape Summary: How does Alectinib, a kinase inhibitor, achieve high-affinity binding to complement protein C1q? is a 0.87 priority gap in neuroinflammation. It has 0 linked hypotheses with average composite score 0.000. Status: partially_addressed.

Key Unanswered Questions

Key Researchers

Colonna, Sevlever, et al. (TREM2 biology)

Clinical Trials

How does Alectinib, a kinase inhibitor, achieve high-affinity binding to complement protein C1q? — INVOKE-2 (completed)

📈 Living Dashboards
0
Hypotheses
0.000
Top Score
0.000
Avg Score
0
Debates
0.00
Avg Quality
60%
Resolution
0
Mechanistic Families
Gap Resolution Progress60%

Hypothesis Score Distribution

🏆 Competing Hypotheses (Ranked by Score)

No hypotheses linked to this gap yet.

🌊 Knowledge Graph Connections

activates (16)

C1q→Microglial PhagocytosisC1q→A1 reactive astrocytesC1q→Microglia-Mediated Synapse LossC1q→microglial CR3 engagementC1q→neuroinflammation
▸ Show 11 more

associated with (9)

C1q→complement-dependent phagocytosisC1q→vulnerable synapses in ADC1q→Complement activationCRP→C1qAlectinib→blood-brain barrier penetration
▸ Show 4 more

binds (1)

C1Q→Alectinib

causes (5)

C1q→SYNAPSE_ELIMINATIONC1q→synaptic dysfunctionC1q→immunosuppressionC1q→synaptic_lossAlectinib→ER stress

contributes to (1)

STAT6-MafB pathway→C1q

enhances (1)

C1q→pro-tumor inflammation

increases risk (1)

C1q→Alzheimer's_disease

inhibits (2)

TYROBP deficiency→C1qC1q→Aβ fibril formation

interact with (1)

33628204→C1q

involved in (1)

C1q→Synaptic Pruning

mediates (3)

C1q→Synaptic TaggingC1q→synaptic pruningC1q→Microglial Synaptic Elimination

produces (2)

tumor-associated macrophages→C1qmicroglia→C1q

regulates (5)

C1q→gC1qRAlectinib→blood_brain_barrierC1q→synaptic stabilityC1q→pruning of stressed neuronsC1q→M2 macrophage polarization

upregulates (2)

ABETA→C1qC1q→Glaucoma
🕑 Activity Feed
✏ update on knowledge_gap by None 2026-04-25T22:15
✏ update on knowledge_gap by None 2026-04-16T22:49
✏ update on knowledge_gap by None 2026-04-16T22:49
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