Transcriptional repressor which plays a role in development of the central nervous system (CNS). In concert with ATXN1 and ATXN1L, involved in brain development. .
In 15 of 15 cancers, the evidence for CIC comes mainly from mutations found in tumours
Each row is a cancer, strongest overall evidence first. The two dots show how strong the inherited (germline) and tumour-mutation (somatic) evidence is; the line between them is the gap.
Inherited (germline) variantsMutations in tumours (somatic)
Scores run from 0 (no evidence) to 1 (strongest). A missing dot at 0 means Open Targets holds no evidence of that kind. Source: Open Targets Platform, fetched live.
Tractability
PROTAC
Half-life Data
gnomAD loss of function constraint: o/e 0.15563000738620758 (upper bound 0.2307800054550171). Low values mean loss of function is poorly tolerated, a safety flag for inhibition.
Who runs trials of these drugs
No named investigators on registry trials of CIC's approved or late-stage drugs in the last three years.
No terminated, withdrawn or suspended trials of CIC's drugs are registered
All 0 drugs and clinical candidates as a table
Each drug, stage and indication links to its Open Targets record, where the trials and approvals behind it are listed. Salt forms (for example a mesylate) are listed as Open Targets records them, as separate entries.