LCK Inhibitors
7 drugsAbout LCK
LCK (lymphocyte-specific protein tyrosine kinase) is a non-receptor tyrosine kinase crucial for T-cell receptor signaling and T cell development. It initiates downstream signaling cascades, leading to T cell activation and immune responses.
Human genetics provide strong validation for LCK as a therapeutic target, with variants linked to severe combined immunodeficiency (score 0.81). Loss-of-function variants increase disease risk, suggesting activation of LCK may be beneficial.
LCK is targeted by 7 FDA-approved small molecule drugs, including Sprycel, Phyrago and Pazopanib Hydrochloride. These drugs are primarily used in oncology (5 drugs) and respiratory diseases (1 drug).
Strategic Insights
ℹ️ How we calculate- White space opportunity in Advanced Malignant Solid Neoplasm with only 3 trials.
- phase2 represents biological uncertainty with 50% completion.
LCK Genetic Evidence Strong
Genetic evidence strongly supports LCK's role in severe combined immunodeficiency (score 0.81).
Strong genetic support increases the likelihood of clinical success for LCK-targeting therapies.
💡 Why activation?
- • Loss-of-function variants increase disease risk (OR > 1) — restoring function may help
- • 100% directional consistency across 2 traits
- • Strong signal in immune system disease, genetic, familial or congenital disease, phenotype pathways
Cross-Disease Effects
Trade-off: LowDirection of Effect
100% alignedEvidence Across Diseases
2 totalGWAS and other genetic studies link LCK to 2 diseases.
Loss-of-function causes disease; activation may help
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 LCK Drugs
Seven companies have approved drugs targeting LCK, including NOVUGEN, Apotex, and Bristol-Myers Squibb.
The presence of multiple players indicates a competitive market, requiring a differentiated therapeutic approach.
| Drug | Company | Approved | Indications |
|---|---|---|---|
| SPRYCEL | Bristol-Myers Squibb | 2006 | 2 |
| VOTRIENT | Novartis | 2009 | 2 |
| PHYRAGO | HANDA THERAP | 2023 | 2 |
| VIZIMPRO | Pfizer | 2018 | 1 |
LCK Drug Modality Landscape
Modalities
Routes of Administration
LCK is amenable to small molecule drugs, with oral options available for convenient dosing.
Exploring alternative modalities like antibodies or PROTACs could provide a competitive advantage.
LCK Clinical Trials 477 trials
Completion by Phase
| Phase | Total | Completed | Failed | Active | Completion |
|---|---|---|---|---|---|
| Phase 1 | 181 | 111 | 47 | 23 | 70% |
| Phase 2 | 238 | 125 | 60 | 52 | 68% |
| Phase 3 | 40 | 26 | 3 | 11 | 90% |
| Phase 4 | 18 | 12 | 1 | 5 | 92% |
Top Sponsors
By Modality
Top Conditions
LCK Drug Approval Timeline (2006 - 2023)
The first LCK-targeting drug was approved in 2006 (Sprycel), with the most recent approval in 2023 (Phyrago).
The continued approval of LCK-targeting drugs suggests ongoing opportunities for innovation in this space.
Pro Intelligence Preview
Deep insights for drug target analysis
Competitive Landscape
- • 6 companies competing
- • Market share by company
Full Drug Portfolio
- • All 7 approved drugs
- • Approval dates & indications
Genetic Validation
- • Full genetic evidence table
- • Effect sizes & directions
Approval Timeline
- • Full 7-drug timeline
- • First-of-modality markers
Clinical Trials Analysis
- • Competition: High (15 sponsors)
- • White space: 10 underexplored indications
- • Success rates by condition
Full summary • All drugs • Genetic evidence • Trials • Timeline
How We Calculate These Metrics
Target Attractiveness Score
A 0-100 score based on trial activity, sponsor diversity, and completion rates. Calculated from 248 clinical trials targeting LCK.
Completion rate: Percentage of trials that reached their planned endpoint. Trials terminated early, withdrawn, or suspended are not counted—these often indicate safety issues, lack of efficacy, or strategic pivots.
- Highly Attractive (80+): High trial activity, many sponsors, strong completion rates
- Attractive (60-79): Good trial activity and validation
- Moderate (40-59): Moderate interest from sponsors
- Low (under 40): Limited trial activity or validation concerns
Strategic Insights
Auto-generated insights based on trial analytics including competition intensity, white space opportunities, modality shifts, and failure patterns. We analyze trial sponsors, phases, indications, and outcomes.
Risk Signals
- High Competition: Many sponsors competing for this target (may reduce market opportunity)
- High Failure Risk: Low trial completion rates suggest development challenges
- Low Validation: Limited trial activity or poor outcomes indicate uncertain viability
- White Space Available: Underexplored indications present opportunities