L-type calcium channel Inhibitors
4 drugsAbout L-type calcium channel
L-type calcium channels are voltage-gated ion channels in excitable cells like heart and smooth muscle. They regulate calcium influx, triggering muscle contraction, hormone secretion, and gene expression.
Human genetic studies strongly support L-type calcium channels as therapeutic targets (max score 0.92). Variants are linked to acquired long QT syndrome (0.92) and Timothy syndrome (0.92), suggesting activation may be beneficial.
Four FDA-approved small molecule drugs target L-type calcium channels, including VERELAN, CLEVIPREX and CARDAMYST. These drugs are used in cardiovascular and other therapeutic areas.
L-type calcium channel Genetic Evidence Strong
L-type calcium channels have strong genetic support with a max score of 0.92 across 42 diseases.
The strong genetic support suggests a higher probability of clinical success for new drugs targeting this channel.
💡 Why activation?
- • Loss-of-function variants increase disease risk (OR > 1) — restoring function may help
- • 100% directional consistency across 2 traits
- • Strong signal in genetic, familial or congenital disease, phenotype pathways
Cross-Disease Effects
Trade-off: LowDirection of Effect
100% alignedEvidence Across Diseases
20 totalGWAS and other genetic studies link CACNA1C to 42 diseases.
Loss-of-function causes disease; activation may help
🔗 Colocalization Evidence 20 strong
max H4: 1.00eQTL/pQTL signals for CACNA1C 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 L-type calcium channel Drugs
Three companies have approved drugs, with AZURITY holding multiple indications for VERELAN.
The market is moderately concentrated, suggesting potential entry barriers for new competitors.
| Drug | Company | Approved | Indications |
|---|---|---|---|
| VERELAN PM | AZURITY | 1998 | 1 |
L-type calcium channel Drug Modality Landscape
Modalities
Routes of Administration
L-type calcium channel is amenable to small molecule drugs, with oral options available for convenient dosing.
Exploring alternative modalities like antibodies or peptides could provide a competitive advantage.
L-type calcium channel Clinical Trials 65 trials
Phase 1-4 trials started in 2008 or later that test an FDA-approved drug acting on L-type calcium channel. Source: ClinicalTrials.gov. How we count
Completion by Phase
| Phase | Total | Completed | Stopped | Active | Completion |
|---|---|---|---|---|---|
| Phase 1 | 23 | 20 | 3 | 0 | 87% |
| Phase 2 | 13 | 8 | 3 | 2 | 73% |
| Phase 3 | 10 | 6 | 3 | 1 | 67% |
| Phase 4 | 19 | 6 | 8 | 4 | 43% |
Top Sponsors
By Modality
Top Conditions
L-type calcium channel Drug Approval Timeline (1990 - 2025)
The first drug was approved in 1990, with the most recent approval in 2025, spanning 36 years.
The continued approvals suggest ongoing interest and potential for further development in this area.
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Deep insights for drug target analysis
Competitive Landscape
- • 3 companies competing
- • Market share by company
Full Drug Portfolio
- • All 4 approved drugs
- • Approval dates & indications
Genetic Validation
- • Full genetic evidence table
- • Effect sizes & directions
Approval Timeline
- • Full 4-drug timeline
- • First-of-modality markers
Clinical Trials Analysis
- • Sponsors: 46 (13 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 L-type calcium channel. A trial counts if an approved drug acting on L-type calcium channel 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.