CD86 Targeted Therapies
2 drugsAbout CD86
CD86 is a protein crucial for T cell activation, a key component of the adaptive immune system. By interacting with CD28 on T cells, it provides a costimulatory signal necessary for full T cell activation. Modulating CD86 activity can effectively dampen the immune response.
Human genetic studies provide strong validation for CD86 as a therapeutic target (max score 0.82). Loss-of-function variants are protective against multiple sclerosis (score 0.82), suggesting inhibition is likely beneficial. CD86 is also genetically linked to lymphoid neoplasm and non-Hodgkin's lymphoma.
CD86 is targeted by 2 FDA-approved fusion protein drugs: ORENCIA and NULOJIX. These drugs are developed by Bristol-Myers Squibb for immune-related indications. The first drug was approved in 2005, with the most recent in 2011.
CD86 Genetic Evidence Strong
CD86 has strong genetic support with a maximum score of 0.82, indicating therapeutic potential.
Strong genetic support increases clinical success probability, especially for inhibition strategies.
💡 Why inhibition?
- • Loss-of-function variants reduce disease risk (OR < 1)
- • 100% directional consistency across 1 traits
- • Strong signal in nervous system disease, immune system disease pathways
Cross-Disease Effects
Trade-off: LowDirection of Effect
100% alignedEvidence Across Diseases
10 totalGWAS and other genetic studies link CD86 to 10 diseases.
Inhibiting this target may be therapeutic
🔗 Colocalization Evidence 20 strong
max H4: 1.00eQTL/pQTL signals for CD86 colocalize with these GWAS traits, providing causal evidence that gene expression changes drive disease risk.
Understanding these scores
Association Score (0-1): Combines all evidence types (genetic, literature, drugs, animal models). Higher = more evidence linking target to disease. This is a ranking heuristic, not a confidence score.
L2G Score: Open Targets uses a machine learning model (Locus-to-Gene) to predict which gene is causal at each GWAS locus. L2G=0.5 means ~50% probability of being the causal gene. Only associations with L2G > 0.05 are included.
Odds Ratio (OR): From gene burden studies (UK Biobank, AstraZeneca PheWAS). Measures how loss-of-function variants affect disease risk. OR<1 = protective (inhibiting target may help), OR>1 = risk (losing function causes disease).
Beta (β): Effect size for continuous traits. β<0 = protective, β>0 = risk.
Clinical Translation (~1.8x): Based on Nelson et al. 2015: drug targets with genetic evidence have ~2x higher success rates in clinical trials. We estimate: Strong support (score ≥0.7) → ~1.8x, Moderate (0.3-0.7) → ~1.3x, Weak → baseline.
Colocalization (H4): Tests whether a GWAS signal and an eQTL/pQTL signal share the same causal variant. H4 is the posterior probability that both traits are associated AND share a causal variant. H4 > 0.8 = strong evidence that gene expression/protein levels drive disease risk. This links genetic variation → gene expression → disease, supporting the target-disease connection.
Top CD86 Drugs
Bristol-Myers Squibb is the only company with approved drugs targeting CD86.
High market concentration indicates potential entry barriers for new competitors.
CD86 Drug Modality Landscape
Modalities
Routes of Administration
CD86 requires biologic approaches (fusion protein), likely due to its structure or location.
The exclusive use of fusion proteins suggests a whitespace opportunity for alternative modalities.
CD86 Clinical Trials 170 trials
Phase 1-4 trials started in 2008 or later that test an FDA-approved drug acting on CD86. Source: ClinicalTrials.gov. How we count
Completion by Phase
| Phase | Total | Completed | Stopped | Active | Completion |
|---|---|---|---|---|---|
| Phase 1 | 39 | 25 | 5 | 9 | 83% |
| Phase 2 | 64 | 34 | 13 | 16 | 72% |
| Phase 3 | 33 | 25 | 1 | 7 | 96% |
| Phase 4 | 34 | 27 | 6 | 1 | 82% |
Top Sponsors
By Modality
Top Conditions
CD86 Drug Approval Timeline (2005 - 2011)
The approval timeline spans 7 years, with the first drug approved in 2005 and the most recent in 2011.
The limited approval activity suggests a potential for renewed innovation in this area.
Pro Intelligence Preview
Deep insights for drug target analysis
Competitive Landscape
- • 1 companies competing
- • Market share by company
Full Drug Portfolio
- • All 2 approved drugs
- • Approval dates & indications
Genetic Validation
- • Full genetic evidence table
- • Effect sizes & directions
Approval Timeline
- • Full 2-drug timeline
- • First-of-modality markers
Clinical Trials Analysis
- • Sponsors: 90 (8 companies)
- • Completion rates by condition
Full summary • All drugs • Genetic evidence • Trials • Timeline
How We Count Trials
- Trials: phase 1-4 interventional trials on ClinicalTrials.gov that started in 2008 or later and test an FDA-approved drug acting on CD86. A trial counts if an approved drug acting on CD86 is in any arm, including as a comparator, and a trial that tests two such drugs counts once. Trials that test only unapproved drugs are not counted. A trial listed as phase 1/2 counts as phase 1, and phase 2/3 as phase 2.
- Active: recruiting, not yet recruiting, enrolling by invitation, or active and no longer recruiting.
- Completion rate: of the trials that have ended, the share marked Completed rather than Terminated or Withdrawn. Completed means the trial ended as planned; it does not mean the drug worked. Suspended trials are not counted as ended.
- Stopped: terminated or withdrawn. Trials stop for many reasons, including slow enrolment and business decisions, not only safety or efficacy.
- Sponsors: the lead sponsor of each trial. Companies are the sponsors ClinicalTrials.gov classes as industry; the rest are universities, hospitals, cooperative groups, government bodies and individuals.