Insulin receptor Analogs
21 drugsAbout Insulin receptor
The Insulin Receptor (INSR) is a transmembrane receptor activated by insulin, regulating glucose metabolism and homeostasis. Upon insulin binding, the receptor activates intracellular signaling cascades, promoting glucose uptake and utilization in target tissues.
INSR is a key therapeutic target validated by strong genetic evidence (max score 0.93) linking loss-of-function variants to diseases like Leprechaunism and insulin-resistance syndrome type A. Activation of INSR is likely beneficial based on genetic data.
There are 20 FDA-approved drugs targeting INSR, primarily biologics (19 drugs) and peptides (1 drug), indicated for metabolic diseases. Top drugs include BASAGLAR, REZVOGLAR and SEMGLEE, marketed by companies like Eli Lilly and Novo Nordisk.
Insulin receptor Genetic Evidence Strong
Strong genetic evidence supports INSR as a drug target, with a maximum score of 0.93.
The strong genetic support suggests a higher probability of clinical success for INSR-targeting drugs.
💡 Why activation?
- • Loss-of-function variants increase disease risk (OR > 1) — restoring function may help
- • 100% directional consistency across 3 traits
- • Strong signal in genetic, familial or congenital disease, endocrine system disease, nutritional or metabolic disease pathways
Cross-Disease Effects
Trade-off: LowDirection of Effect
100% alignedEvidence Across Diseases
20 totalGWAS and other genetic studies link INSR to 43 diseases.
Loss-of-function causes disease; activation may help
Loss-of-function causes disease; activation may help
🔗 Colocalization Evidence 20 strong
max H4: 1.00eQTL/pQTL signals for INSR 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 Insulin receptor Drugs
Seven companies have approved drugs targeting INSR, with Eli Lilly and Novo Nordisk as leading players.
The concentrated market share of Eli Lilly and Novo Nordisk indicates high barriers to entry for new competitors.
| Drug | Company | Approved | Indications |
|---|---|---|---|
| XULTOPHY 100/3.6 | Novo Nordisk | 2016 | 2 |
| SOLIQUA 100/33 | SANOFI-AVENTIS US | 2016 | 2 |
| LYUMJEV | Eli Lilly | 2020 | 1 |
| MERILOG | SANOFI-AVENTIS U.S. LLC | 2025 | 1 |
| MERILOG SOLOSTAR | SANOFI-AVENTIS U.S. LLC | 2025 | 1 |
| NOVOLOG | Novo Nordisk | 2000 | 1 |
| TRESIBA | Novo Nordisk | 2015 | 1 |
| MYXREDLIN | Baxter | 2019 | 1 |
| LANTUS | Sanofi | 2000 | 1 |
| HUMALOG KWIKPEN | Eli Lilly | 1996 | 1 |
| HUMALOG | Eli Lilly | 1996 | 1 |
| LEVEMIR | Novo Nordisk | 2005 | 1 |
| ZYKADIA | Novartis | 2014 | 1 |
| FIASP PENFILL | Novo Nordisk | 2017 | 1 |
| FIASP | Novo Nordisk | 2017 | 1 |
| FIASP FLEXTOUCH | Novo Nordisk | 2017 | 1 |
| NOVOLOG MIX 70/30 | Novo Nordisk | 2001 | 1 |
| ADLYXIN | SANOFI-AVENTIS US | 2016 | - |
Insulin receptor Drug Modality Landscape
Modalities
Routes of Administration
Insulin receptor requires biologic approaches (biologic (other)), likely due to its structure or location.
The dominance of biologics suggests a potential whitespace opportunity for novel small molecule INSR activators.
📈 Modality Evolution
other biologics pioneered Insulin receptor targeting (1996), with peptides entering more recently (2016).
Insulin receptor Clinical Trials 1,036 trials
Phase 1-4 trials started in 2008 or later that test an FDA-approved drug acting on Insulin receptor. Source: ClinicalTrials.gov. How we count
Completion by Phase
| Phase | Total | Completed | Stopped | Active | Completion |
|---|---|---|---|---|---|
| Phase 1 | 309 | 277 | 18 | 14 | 94% |
| Phase 2 | 158 | 106 | 29 | 22 | 79% |
| Phase 3 | 296 | 265 | 17 | 14 | 94% |
| Phase 4 | 273 | 214 | 33 | 26 | 87% |
Top Sponsors
By Modality
Top Conditions
Top Drugs
Phase 3 Readout Calendar Pro
2 Phase 3 trials testing approved Insulin receptor drugs across all sponsors.
Coverage: trials whose intervention is an approved drug targeting Insulin receptor. Pre-approval candidates with development codes (e.g. AZD0901, MK-7240) are not yet linked. Anchored on CT.gov primary completion date.
Insulin receptor Drug Approval Timeline (1996 - 2025)
The first INSR-targeting drug was approved in 1996, with the most recent approval in 2025, spanning 30 years.
The continued approval of INSR-targeting drugs suggests sustained interest and potential for further innovation in this area.
Pro Intelligence Preview
Deep insights for drug target analysis
Competitive Landscape
- • 8 companies competing
- • Market share by company
Full Drug Portfolio
- • All 21 approved drugs
- • Approval dates & indications
Genetic Validation
- • Full genetic evidence table
- • Effect sizes & directions
Approval Timeline
- • Full 21-drug timeline
- • First-of-modality markers
Clinical Trials Analysis
- • Sponsors: 318 (77 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 Insulin receptor. A trial counts if an approved drug acting on Insulin receptor 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.