🧫
FK866 treatment in DSS-induced colitis mouse model
active
experiment
Created: 2026-04-10T14:44:04
By: etl-v1-backfill
Quality:
50%
✓ SciDEX
ID: exp-ecdfc305-fcd8-4767-b8cd-a70c9cfa9834
🧫 Experiment Protocol
ValidationInflammatory bowel disease (colitis)NAMPTDSS-induced colitis miceproposed
Investigation of the therapeutic effects of FK866, a NAMPT inhibitor, in a dextran sulfate sodium (DSS)-induced colitis mouse model. The study examined how FK866 treatment affects inflammatory markers, NAD metabolism, and disease severity in acute intestinal inflammation. The experiment demonstrated that FK866 ameliorated colitis symptoms by reducing mucosal NAD levels, inhibiting NAD-dependent enzymes (PARP1, Sirt6, CD38), decreasing NF-κB activation, and reducing inflammatory cell infiltration including monocytes, macrophages, and activated T cells. The mechanism was linked to altered macrophage polarization with reduced pro-inflammatory markers (CD86, CD38, MHC-II, IL-6) and increased anti-inflammatory markers (CD206, Egr2, IL-10).
PRIMARY OUTCOME
Colitis severity and inflammatory markers
EXPECTED OUTCOMES
FK866 would reduce inflammation by depleting NAD and inhibiting inflammatory pathways
SUCCESS CRITERIA
Reduced colitis severity, decreased inflammatory markers, and altered immune cell populations
PROTOCOL
DSS administration to induce colitis followed by FK866 treatment with assessment of mucosal NAD levels, enzyme activities, inflammatory cell infiltration, and cytokine production
LINKED HYPOTHESES
Source: PMID 28877980 ↗
🧫 Experiment Extras
PATHWAY
NAD salvage pathway, NF-κB signaling
MARKET PRICE
$0.50
STATUS
proposed
▸Metadataorigin_type: v1_polymorphic_backfill
| origin_type | v1_polymorphic_backfill |
| source_table | experiments |
| _schema_version | 1 |
📊 Evidence Profile
Evidence Balance
+0%
Certainty
0%
Debates
0
Incoming
0
Outgoing
0
0 supporting
0 contradicting
0 neutral
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