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.
Human 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 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 |
|---|---|---|---|
| PAZOPANIB HYDROCHLORIDE | Teva | 2023 | 2 |
| SPRYCEL | Bristol-Myers Squibb | 2006 | 2 |
| VOTRIENT | Novartis | 2009 | 2 |
| VIZIMPRO | Pfizer | 2018 | 1 |
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.
Clinical Trials 531 trials
Completion by Phase
| Phase | Total | Completed | Failed | Active | Completion |
|---|---|---|---|---|---|
| Phase 1 | 201 | 126 | 48 | 27 | 72% |
| Phase 2 | 257 | 135 | 63 | 57 | 68% |
| Phase 3 | 52 | 34 | 4 | 14 | 89% |
| Phase 4 | 21 | 14 | 2 | 5 | 88% |
Top Sponsors
By Modality
Top Conditions
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
- • 7 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