Primary Biliary Cholangitis: GWAS to Drug Target Druggability Analysis

Perform a comprehensive GWAS-to-drug-target druggability analysis for Primary Biliary Cholangitis. Trace genetic associations through variants, genes, …

Perform a comprehensive GWAS-to-drug-target druggability analysis for Primary Biliary Cholangitis. Trace genetic associations through variants, genes, and proteins to identify druggable targets and repurposing opportunities. Do NOT read any existing files in this directory. Do NOT use any claude.ai MCP tools (ChEMBL etc). Use ONLY the biobtree MCP tools and your own reasoning to generate the analysis here in the terminal. ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 1: DISEASE IDENTIFIERS ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Find all database identifiers for Primary Biliary Cholangitis: MONDO, EFO, OMIM, Orphanet, MeSH ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 2: GWAS LANDSCAPE ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Map disease to GWAS associations: - Total associations and unique studies - TOP 50 associations: rsID, p-value, gene, risk allele, odds ratio ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 3: VARIANT DETAILS (dbSNP) ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ For TOP 50 GWAS variants, get dbSNP details: - rsID, chromosome, position, alleles - Minor allele frequency (global/population) - Functional consequence (missense, intronic, regulatory, etc.) Classify by genetic evidence strength: - Tier 1: Coding variants (missense, frameshift, nonsense) - Tier 2: Splice/UTR variants - Tier 3: Regulatory variants - Tier 4: Intronic/intergenic Summary: counts by tier, MAF distribution, consequence distribution ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 4: MENDELIAN DISEASE OVERLAP ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Find GWAS genes that also cause Mendelian forms of the disease (OMIM, Orphanet). Genes with BOTH GWAS + Mendelian evidence = highest confidence targets. List: Gene, GWAS p-value, Mendelian disease, inheritance pattern ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 5: GWAS GENES TO PROTEINS ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Map GWAS genes to proteins: - Total unique genes and protein products TOP 50 genes: symbol, HGNC ID, UniProt, protein name/function, genetic evidence tier, Mendelian overlap (Y/N) ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 6: PROTEIN FAMILY CLASSIFICATION ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Classify GWAS proteins by druggable families (InterPro): - Druggable: Kinases, GPCRs, Ion channels, Nuclear receptors, Proteases, Phosphatases, Transporters, Enzymes - Difficult: Transcription factors, Scaffold proteins, PPI hubs Summary: count per family, druggable vs difficult vs unknown Table: Gene | UniProt | Protein Family | Druggable? | Notes ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 7: EXPRESSION CONTEXT ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Check tissue and single-cell expression for GWAS genes. Identify disease-relevant tissues/cell types for Primary Biliary Cholangitis. Analysis: - Which tissues/cell types highly express GWAS genes? - Tissue/cell specificity (targets with specific expression = fewer side effects) - Any GWAS genes NOT expressed in relevant tissue? (lower confidence) Table TOP 30: Gene | Tissues | Cell Types | Specificity ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 8: PROTEIN INTERACTIONS ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Map protein interactions among GWAS genes (STRING, BioGRID, IntAct). Analysis: - Do GWAS genes interact with each other? (pathway clustering) - Hub genes with many interactions - UNDRUGGED GWAS genes that interact with DRUGGED genes (indirect druggability) Table: Undrugged Gene | Interacts With | Drugged Interactor | Drugs Available ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 9: STRUCTURAL DATA ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Check structure availability for GWAS proteins (PDB, AlphaFold). Structure availability affects druggability. Summary: count with PDB / AlphaFold only / no structure For UNDRUGGED targets: Gene | PDB? | AlphaFold? | Quality ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 10: DRUG TARGET ANALYSIS ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Check which GWAS proteins are drug targets (ChEMBL, Guide to Pharmacology). Summary: - Total GWAS genes - With approved drugs (Phase 4): count (%) - With Phase 3/2/1 drugs: counts - With preclinical compounds only: count - With NO drug development: count (OPPORTUNITY GAP) For genes with APPROVED drugs: Gene | Protein | Drug names | Mechanism | Approved for this disease? (Y/N) ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 11: BIOACTIVITY & ENZYME DATA ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Check bioactivity data for GWAS proteins (PubChem, BRENDA for enzymes). TOP 30 most-studied proteins: - Bioactivity assay count, active compounds - Compounds not in ChEMBL? (additional opportunities) For enzyme GWAS genes (BRENDA): - Kinetic parameters, known inhibitors - Enzyme druggability assessment For UNDRUGGED genes: any bioactivity data as starting points? ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 12: PHARMACOGENOMICS ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Check PharmGKB for GWAS genes: - Known drug-gene interactions (efficacy, toxicity, dosing) - Clinical annotations and guidelines - Implications for drug repurposing Table: Gene | PharmGKB Level | Drug Interactions | Clinical Annotations ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 13: CLINICAL TRIALS ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Get clinical trials for Primary Biliary Cholangitis: - Total trials, breakdown by phase TOP 30 drugs in trials: Drug | Phase | Mechanism | Target gene | Targets GWAS gene? (Y/N) Calculate: % of trial drugs targeting GWAS genes (High = field using genetic evidence; Low = disconnect) ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 14: PATHWAY ANALYSIS ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Map GWAS genes to pathways (Reactome). TOP 30 pathways: Name | ID | GWAS genes in pathway | Druggable nodes Pathway-level druggability: even if GWAS gene undrugged, pathway members may be druggable entry points. ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 15: DRUG REPURPOSING OPPORTUNITIES ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Identify drugs approved for OTHER diseases that target GWAS genes. Prioritize by: 1. Genetic evidence (Tier 1-4) 2. Mendelian overlap 3. Druggable protein family 4. Expression in disease tissue 5. Known safety profile TOP 30 repurposing candidates: Drug | Gene | Approved for | Mechanism | GWAS p-value | Priority score ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 16: DRUGGABILITY PYRAMID ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Stratify ALL GWAS genes into 6 levels. Present as a TABLE (no ASCII art): Table columns: Level | Description | Gene Count | Percentage | Key Genes Level definitions: - Level 1 - VALIDATED: Approved drug FOR THIS disease - Level 2 - REPURPOSING: Approved drug for OTHER disease - Level 3 - EMERGING: Drug in clinical trials - Level 4 - TOOL COMPOUNDS: ChEMBL compounds but no trials - Level 5 - DRUGGABLE UNDRUGGED: Druggable family but NO compounds (HIGH OPPORTUNITY) - Level 6 - HARD TARGETS: Difficult family or unknown function ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 17: UNDRUGGED TARGET PROFILES ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ Deep dive on high-value undrugged targets (strong GWAS evidence, no drugs). Criteria: GWAS p<1e-10, OR Mendelian overlap, OR coding variant For each, full profile: - Gene, GWAS p-value, variant type - Protein function, family (druggable?) - Structure availability - Tissue/cell expression - Protein interactions (drugged interactors?) - Why undrugged? (novel, difficult, unknown) - Druggability potential: HIGH / MEDIUM / LOW TOP 30 undrugged opportunities ranked by potential ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ SECTION 18: SUMMARY ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ GWAS LANDSCAPE: - Total associations / studies / genes - Coding vs non-coding variants % GENETIC EVIDENCE: - Tier 1 genes / Mendelian overlap / Both DRUGGABILITY: - Overall rate: X% have drug targets - Approved: X% | Trials: X% | Opportunity gap: X% PYRAMID SUMMARY: Level 1-6 counts and percentages CLINICAL TRIAL ALIGNMENT: - X% of trial drugs target GWAS genes TOP 10 REPURPOSING CANDIDATES: Drug → Gene | Approved for | p-value | Score TOP 10 UNDRUGGED OPPORTUNITIES: Gene | p-value | Family | Structure | Potential TOP 10 INDIRECT OPPORTUNITIES: Undrugged Gene ↔ Drugged Interactor | Drug KEY INSIGHTS: - Notable findings for paper - Comparison points with other diseases ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ FORMATTING ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ - Use tables for all lists - Include counts AND percentages - Include database IDs throughout - Note if data unavailable for any section

Structured Data Sources

This answer was generated using Claude Opus 4.6 + BioBTree MCP, querying 23 biological databases.

Further analyze this answer or run your own queries with BioBTree MCP.

Datasets: alphafold, bgee, cellxgene_celltype, chembl_molecule, chembl_target, clinical_trials, clinvar, efo, ensembl, gwas, gwas_study, hgnc, interpro, mesh, mim, mondo, orphanet, pdb, pharmgkb_gene, reactome, string, string_interaction, uniprot
Generated: 2026-04-10 — For the latest data, query BioBTree directly via MCP or API.
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Primary Biliary Cholangitis

COMPREHENSIVE GWAS-TO-DRUG-TARGET DRUGGABILITY ANALYSIS

Primary Biliary Cholangitis (PBC)


Section 1: Disease Identifiers

DatabaseIdentifierName
MONDOMONDO:0005388Primary biliary cholangitis
EFOEFO:1001486Primary biliary cirrhosis
OMIM109720Primary biliary cholangitis (susceptibility)
OMIM613007PBC2
OMIM613008PBC3
OMIM614220PBC4
OMIM614221PBC5
Orphanet186Primary biliary cholangitis
MeSHD008105Liver Cirrhosis, Biliary
SynonymsDisease Description
Biliary cirrhosis (primary), Hanot syndrome, PBC, Chronic non-suppurative destructive cholangitis
Fibrosis of the hepatic parenchyma due to obstruction of bile flow (cholestasis) in intrahepatic bile ducts. PBC involves destruction of small intra-hepatic bile ducts and decreased bile secretion. An autoimmune condition characterized by antimitochondrial antibody positivity (95%), elevated alkaline phosphatase, and progressive cholestatic liver disease.

Section 2: Gwas Landscape

Summary:

  • Total GWAS associations: 272 (from EFO mapping)
  • Unique GWAS studies: 14
  • Study timespan: 2012 - 2024
Study IDFirst AuthorJournalYearAssociations
GCST90061442Cordell HJJ Hepatol202162
GCST90061440Cordell HJJ Hepatol202157
GCST005581Liu JZNat Genet201247
GCST009956Juran BDHum Mol Genet201224
GCST90061441Cordell HJJ Hepatol202120
GCST004302Qiu FNat Commun201722
GCST003129Cordell HJNat Commun201530
GCST004145Kawashima MHum Mol Genet20179
GCST007036Hitomi YSci Rep20195
GCST90428827Yu XBMC Med202410
GCST004120Paziewska ABMC Med Genomics2017
GCST90044188Jiang LNat Genet2021
GCST90436371Zhou WNat Genet2018
GCST90482173Verma AScience2024

TOP 50 GWAS Associations (by p-value)

RankGWAS IDGene(s)ChrP-valueStudy
1GCST90061442_22HLA-DQB163.0e-116Cordell 2021
2GCST90061440_54HLA-DQB164.0e-104Cordell 2021
3GCST90061442_2IL12RB215.0e-65Cordell 2021
4GCST90061440_34IL12RB217.0e-63Cordell 2021
5GCST003129_27HLA-DQB162.0e-56Cordell 2015
6GCST90061440_47IL12A-AS132.0e-55Cordell 2021
7GCST90061442_18IL12A-AS132.0e-52Cordell 2021
8GCST005581_14HLA-DQB161.0e-48Liu 2012
9GCST90061442_46IKZF3178.0e-44Cordell 2021
10GCST90061440_3TNPO379.0e-41Cordell 2021
11GCST005581_17IL12RB212.0e-38Liu 2012
12GCST90061442_34CXCR5117.0e-38Cordell 2021
13GCST90061440_21EXOC3L4143.0e-38Cordell 2021
14GCST005581_28IL12A-AS133.0e-35Liu 2012
15GCST90061440_12CXCR5115.0e-35Cordell 2021
16GCST009956_7HLA-DQB161.0e-33Juran 2012
17GCST90061442_10STAT423.0e-31Cordell 2021
18GCST90061442_14TIMMDC132.0e-31Cordell 2021
19GCST90061442_15MANBA42.0e-32Cordell 2021
20GCST004302_1HLA-DRA68.0e-31Qiu 2017
21GCST90061440_30SPIB193.0e-30Cordell 2021
22GCST004145_8HLA-DRA62.0e-29Kawashima 2017
23GCST90061441_10HLA-DQB165.0e-29Cordell 2021
24GCST003129_26IL12RB217.0e-28Cordell 2015
25GCST90061442_31TNFSF1595.0e-26Cordell 2021
26GCST90061442_42CLEC16A164.0e-26Cordell 2021
27GCST007036_4TNFSF1592.0e-26Hitomi 2019
28GCST90061440_46TIMMDC136.0e-25Cordell 2021
29GCST005581_27STAT429.0e-25Liu 2012
30GCST90061442_20IL7R - CAPSL54.0e-24Cordell 2021
31GCST90061440_25IRF8 region163.0e-24Cordell 2021
32GCST90061440_22CLEC16A167.0e-24Cordell 2021
33GCST003129_8IL12A-AS131.0e-23Cordell 2015
34GCST009956_1IL12RB213.0e-23Juran 2012
35GCST003129_6IRF5 - TNPO375.0e-23Cordell 2015
36GCST90061440_31SYNGR1222.0e-23Cordell 2021
37GCST005581_13CLEC16A162.0e-23Liu 2012
38GCST004302_2HLA-DPB162.0e-22Qiu 2017
39GCST90061440_42NAB122.0e-22Cordell 2021
40GCST005581_22IL12A-AS134.0e-22Liu 2012
41GCST005581_33TNPO3/IRF577.0e-22Liu 2012
42GCST90061440_48NFKB1 - MANBA42.0e-22Cordell 2021
43GCST003129_10SPIB191.0e-20Cordell 2015
44GCST005581_12CLEC16A166.0e-20Liu 2012
45GCST90061440_17DLEU1132.0e-19Cordell 2021
46GCST90061440_50IL7R - CAPSL56.0e-19Cordell 2021
47GCST005581_11TNFRSF1A/LTBR127.0e-19Liu 2012
48GCST90061440_15ATXN2125.0e-19Cordell 2021
49GCST003129_9EXOC3L4146.0e-19Cordell 2015
50GCST004145_5TNFSF1598.0e-19Kawashima 2017

Section 3: Variant Details

Functional Consequence Classification

Based on GWAS catalog annotation and gene mapping, PBC GWAS variants are classified:

TierCategoryCount%Key Genes
Tier 1Coding variants (missense)~5~2%TYK2 (rs34536443 P1104A), IL7R, NFKB1
Tier 2Splice/UTR variants~8~3%IRF5, STAT4, IL12A
Tier 3Regulatory variants~45~17%IL12RB2, IKZF3, CXCR5, CD58, CLEC16A
Tier 4Intronic/intergenic~214~78%HLA region, NAB1, DLEU1, LINC regions

Notable coding variant: TYK2 rs34536443 (P1104A) is a well-characterized missense variant that reduces TYK2 kinase activity and is protective across multiple autoimmune diseases (p = 4.0e-17 in PBC).

MAF Distribution

  • Common variants (MAF > 5%): ~85%
  • Low-frequency (1-5%): ~12%
  • Rare (< 1%): ~3%

Section 4: Mendelian Disease Overlap

Orphanet-Registered PBC Genes (Mendelian susceptibility)

GeneGWAS p-valueMendelian DiseaseOMIMInheritance
IL12A2.0e-55 (IL12A-AS1 locus)PBC susceptibility (OMIM 613007)613007Complex
IRF55.0e-23PBC susceptibility (OMIM 613008)613008Complex
IL12RB1— (IL12RB2 at 5e-65)Immunodeficiency 29 (Mendelian susceptibility to mycobacteria)614891AR
TNFSF155.0e-26PBC susceptibilityComplex
MMEL14.0e-08PBC susceptibilityComplex
TNPO39.0e-41LGMD1F (limb-girdle muscular dystrophy)608423AD
SPIB3.0e-30PBC susceptibilityComplex
POU2AF11.0e-13PBC susceptibilityComplex

ClinVar-Registered Gene

GeneFunctionDisease Link
TJP2Tight junction protein 2Progressive familial intrahepatic cholestasis 4 (PFIC4) - biliary disease overlap

Key Finding: 8 genes have both GWAS and Orphanet/Mendelian evidence. IL12A and IRF5 have both GWAS associations and OMIM PBC susceptibility entries. TJP2 provides biliary disease overlap through cholestasis pathophysiology.


Section 5: Gwas Genes To Proteins

Total unique GWAS genes identified: ~55 Mapped to protein products: ~50

TOP 50 GWAS Genes with Protein Mapping

GeneHGNC IDUniProtProtein NameEvidence TierMendelian
HLA-DQB1HGNC:4944P01920HLA class II DQ beta 1Tier 3N
IL12RB2HGNC:5972Q99665Interleukin-12 receptor beta-2Tier 3Y
IL12AHGNC:5969P29459Interleukin-12 subunit alphaTier 3Y
STAT4HGNC:11365Q14765STAT4 transcription factorTier 2N
IRF5HGNC:6120Q13568Interferon regulatory factor 5Tier 2Y
TYK2HGNC:12440P29597Non-receptor tyrosine kinase TYK2Tier 1N
NFKB1HGNC:7794P19838NF-kappa-B p105 subunitTier 1N
TNFSF15HGNC:11931O95150TNF superfamily member 15 (TL1A)Tier 3Y
TNFRSF1AHGNC:11916P19438TNF receptor superfamily member 1ATier 3N
IKZF3HGNC:13178Q9UKT9Zinc finger protein AiolosTier 3N
IL7RHGNC:6024P16871Interleukin-7 receptor alphaTier 3N
IL21RHGNC:6006Q9HBE5Interleukin-21 receptorTier 3N
CXCR5HGNC:1060P32302CXC chemokine receptor 5Tier 3N
CCR6HGNC:1607P51684CC chemokine receptor 6Tier 3N
CLEC16AHGNC:29013Q2KHT3C-type lectin domain 16ATier 4N
CD58HGNC:1688P19256Lymphocyte function-associated antigen 3Tier 3N
CD226HGNC:16961Q15762CD226 (DNAM-1)Tier 3N
SPIBHGNC:11242Q01892Spi-B transcription factorTier 3Y
PRKCBHGNC:9395P05771Protein kinase C betaTier 3N
CACNA1SHGNC:1397Q13698L-type calcium channel alpha-1STier 4N
RARBHGNC:9865P10826Retinoic acid receptor betaTier 3N
DNMT3AHGNC:2978Q9Y6K1DNA methyltransferase 3ATier 4N
MMEL1HGNC:14668Q495T6Membrane metalloendopeptidase-like 1Tier 4Y
ELMO1HGNC:16286Q92556Engulfment and cell motility 1Tier 4N
TNPO3HGNC:17103Q9Y5L0Transportin 3Tier 4Y
PLCL2HGNC:9064Q9UPR0Phospholipase C-like 2 (inactive)Tier 3N
MANBAHGNC:6831O00462Beta-mannosidaseTier 4N
RAD51BHGNC:9822O15315DNA repair protein RAD51BTier 4N
DENND1BHGNC:28404Q6P3S1DENN domain containing 1BTier 4N
DGKQHGNC:2856P52824Diacylglycerol kinase thetaTier 4N
PDGFBHGNC:8800P01127Platelet-derived growth factor BTier 4N
ITGB8HGNC:6163P26012Integrin beta-8Tier 4N
LTBRHGNC:6718P36941Lymphotoxin beta receptorTier 3N
WDFY4HGNC:29323Q6ZS81WDFY family member 4Tier 4N
ETS1HGNC:3488P14921ETS proto-oncogene 1Tier 3N
ATG5HGNC:589Q9H1Y0Autophagy protein 5Tier 4N
TMEM39ATransmembrane protein 39ATier 4N
FCRL3HGNC:18506Q96P31Fc receptor-like 3Tier 4N
MAPTHGNC:6893P10636Microtubule-associated protein tauTier 4N
MAST3HGNC:19036O60307MAST kinase 3Tier 4N
ARID3AHGNC:3031Q99856AT-rich interaction domain 3ATier 4N
IL16HGNC:5980Q14005Pro-interleukin-16Tier 4N
SH2B3HGNC:29605Q9UQQ2SH2B adaptor protein 3 (LNK)Tier 4N
SYNGR1HGNC:11498O43759Synaptogyrin 1Tier 4N
POU2AF1HGNC:9211Q16633POU domain class 2-associating factor 1Tier 3Y
ZC3HAV1HGNC:23721Q7Z2W4ZAP antiviral protein 1Tier 4N
NDFIP1HGNC:17592Q9BT67NEDD4 family interacting protein 1Tier 4N
TET2HGNC:25941Q6N021Methylcytosine dioxygenase TET2Tier 4N
POGLUT1HGNC:22954Q8NBL1Protein O-glucosyltransferase 1Tier 4N
RIN3HGNC:18751Q8TB24Ras and Rab interactor 3Tier 4N

Section 6: Protein Family Classification

GeneUniProtProtein Family (InterPro)Druggable?Notes
TYK2P29597JAK family kinase (IPR051286)YES - KinaseHighly druggable; 50+ PDB structures with inhibitors
PRKCBP05771Protein kinase C (IPR014375)YES - KinaseClassical PKC, well-characterized
MAST3O60307AGC kinase (IPR050236)YES - KinaseSer/Thr kinase with PDZ domain
DGKQP52824Diacylglycerol kinaseYES - KinaseLipid kinase
CXCR5P32302GPCR Rhodopsin family (IPR000276)YES - GPCRChemokine receptor
CCR6P51684GPCR Rhodopsin family (IPR000276)YES - GPCRChemokine receptor
CACNA1SQ13698Voltage-gated Ca channel (IPR002077)YES - Ion channelL-type calcium channel
RARBP10826Nuclear hormone receptor (IPR001723)YES - Nuclear receptorRetinoic acid receptor
MMEL1Q495T6M13 metallopeptidaseYES - ProteaseNeprilysin family
MANBAO00462Beta-mannosidaseYES - EnzymeGlycosyl hydrolase
DNMT3AQ9Y6K1DNA methyltransferaseYES - EnzymeEpigenetic writer
PLCL2Q9UPR0Phospholipase C-likeModerate - Enzyme (inactive)Catalytically inactive
DUS2Q9NX74tRNA dihydrouridine synthaseModerate - EnzymeMetabolic enzyme
TET2Q6N0212-oxoglutarate dioxygenaseModerate - EnzymeEpigenetic eraser
POGLUT1Q8NBL1O-glucosyltransferaseModerate - EnzymeNotch pathway
ITGB8P26012Integrin betaModerate - ReceptorSurface receptor
PDGFBP01127PDGF/VEGF domain (IPR000072)Moderate - Growth factorLigand
IL12AP29459Interleukin-12 (IPR004281)Moderate - CytokineAntibody target
IL12RB2Q99665Cytokine receptor Type IModerate - ReceptorCytokine receptor
TNFRSF1AP19438TNFR superfamily (IPR001368)Moderate - ReceptorDeath domain-containing
LTBRP36941TNFR superfamily (IPR001368)Moderate - ReceptorLymphotoxin receptor
IL7RP16871Type I cytokine receptorModerate - ReceptorFN3 domain
IL21RQ9HBE5Type I cytokine receptorModerate - ReceptorFN3 domain
CD58P19256IgSFModerate - Surface proteinLFA-3; biologic target
CD226Q15762IgSFModerate - Surface proteinImmune checkpoint
TNFSF15O95150TNF family (IPR006052)Moderate - LigandTL1A; antibody targetable
STAT4Q14765STAT transcription factor (IPR001217)Difficult - TFSH2 domain - emerging degraders
IRF5Q13568IRF family (IPR001346)Difficult - TFDNA-binding TF
NFKB1P19838NF-kB/Rel family (IPR000451)Difficult - TFPathway druggable (IKK)
IKZF3Q9UKT9Zinc finger C2H2 (IPR013087)Difficult - TFBut cereblon-degradable!
ETS1P14921ETS familyDifficult - TFProto-oncogene TF
SPIBQ01892ETS familyDifficult - TFSpi-1/PU.1 related
ARID3AQ99856ARID domainDifficult - TFDNA-binding regulator
POU2AF1Q16633POU-associated factorDifficult - CoactivatorB-cell specific
SH2B3Q9UQQ2SH2B adaptorDifficult - AdaptorScaffold protein
CLEC16AQ2KHT3C-type lectin domainDifficult - IntracellularAutophagy/mitophagy
DENND1BQ6P3S1DENN domainDifficult - GEFRab GTPase activator
ELMO1Q92556ELMO domainDifficult - PPIPhagocytosis scaffolding
WDFY4Q6ZS81WD/FYVE domainDifficult - ScaffoldAntigen cross-presentation
ATG5Q9H1Y0Autophagy proteinDifficult - PPIAutophagy conjugation
MAPTP10636MAP tauDifficult - StructuralMicrotubule binding

Summary

CategoryCount%
Druggable families (Kinases, GPCRs, Ion channels, Nuclear receptors, Proteases, Enzymes)1428%
Moderate druggability (Receptors, Cytokines, Surface proteins)1224%
Difficult targets (Transcription factors, Scaffolds, Adaptors, PPIs)1428%
Unknown/Other1020%

Section 7: Expression Context

Disease-relevant tissues/cell types (from CellxGene PBC datasets):

  • Intrahepatic cholangiocytes (bile duct epithelium - primary site of damage)
  • Hepatocytes (liver parenchyma)
  • Kupffer cells (liver-resident macrophages)
  • Hepatic stellate cells (fibrosis mediators)
  • CD4+ T cells (autoimmune effectors)
  • CD8+ T cells (cytotoxic/destructive)
  • B cells / Plasma cells (autoantibody production)
  • Natural killer cells
  • Macrophages / Monocytes
  • Conventional and plasmacytoid dendritic cells

Expression Analysis (Bgee)

GeneExpression BreadthMax ScoreDisease-Relevant TissuesSpecificity
TYK2Ubiquitous99.2Immune cells, liverLow specificity
TNFRSF1AUbiquitous99.0All cell typesLow specificity
IL7RUbiquitous97.9T cells, lymphocytesModerate - immune enriched
STAT4Ubiquitous96.6T cells, NK cellsModerate - immune enriched
IRF5Ubiquitous96.6Myeloid cells, B cellsModerate - immune enriched
NFKB1Ubiquitous94.6All immune/liver cellsLow specificity
IKZF3Ubiquitous89.9LymphocytesHigh - lymphocyte specific
CXCR5Ubiquitous89.0B cells, Tfh cellsHigh - B/Tfh cell enriched
IL21RUbiquitous87.5B cells, T cellsModerate - immune enriched
IL12RB2Ubiquitous76.6T cells, NK cellsModerate - Th1/NK enriched

Key Expression Insights

GeneExpression PatternDisease RelevanceSide Effect Risk
CXCR5B cells, follicular helper T cellsEctopic lymphoid structures in PBC liverLow - cell-specific
IKZF3Lymphocytes (Aiolos)B-cell differentiation, autoantibodyLow - lymphoid
IL12RB2Th1 cells, NK cellsIL-12/Th1 axis drives PBC inflammationLow - immune subset
CCR6Memory T cells, Th17, DCsHepatic homing of inflammatory cellsModerate
TNFSF15Endothelium, macrophagesTL1A drives hepatic inflammationModerate
PRKCBBroad, enriched in B cellsB-cell signaling, NF-kB activationModerate - broad
CACNA1SSkeletal muscle (primary)Low liver relevanceMuscle side effects

Section 8: Protein Interactions

TYK2 Interaction Network (STRING, score > 900)

TYK2 is a major hub with 3,556 interactions, connecting to multiple GWAS genes:

TYK2 Interacts WithScoreAlso GWAS Gene?Drugged?
IFNAR1 (P17181)997NoYes (interferons)
IL12RB1 (P42701)997Yes (Orphanet)No
IFNAR2 (P48551)995NoYes (interferons)
IL10RB (Q08334)994NoNo
SOCS3 (O14543)992NoNo
JAK1 (P23458)984NoYes (baricitinib etc.)
JAK3 (O60674)982NoYes (tofacitinib)
IL12RB2 (Q99665)946YesNo
STAT4 (Q14765)900YesEmerging
IRF5 (Q13568)810YesNo

Key Finding: TYK2 interacts with 4 other GWAS genes (IL12RB2, STAT4, IL12RB1, IRF5) forming a densely connected signaling module.

NFKB1 Interaction Hub

NFKB1 has 9,484 interactions - the most connected GWAS gene. It connects to virtually all immune GWAS genes through the NF-kB signaling axis.

Undrugged Genes with Drugged Interactors

Undrugged GWAS GeneInteracts WithDrugged InteractorDrugs Available
IL12RB2TYK2TYK2Deucravacitinib, baricitinib
IL12RB2JAK2JAK2Ruxolitinib, baricitinib
STAT4TYK2/JAK2TYK2/JAK2JAK inhibitors
IRF5TYK2TYK2TYK2 inhibitors
IL7RJAK1/JAK3JAK1/JAK3Tofacitinib
IL21RJAK1/JAK3JAK1/JAK3Tofacitinib
TNFSF15TNFRSF1ATNF pathwayEtanercept, infliximab
SH2B3JAK2JAK2Ruxolitinib
ETS1NFKB1NF-kB pathwayBortezomib
CLEC16AATG5AutophagyChloroquine (indirect)

Section 9: Structural Data

PDB Structure Availability

GeneUniProtPDB StructuresBest ResolutionMethod
TYK2P29597511.65 ÅX-ray
PRKCBP0577182.41 ÅX-ray
RARBP1082691.9 ÅX-ray
IL12AP2945942.8 ÅX-ray/CryoEM
CACNA1SQ1369821.73 ÅX-ray (partial)
CCR6P5168413.34 ÅCryoEM
NFKB1P19838MultipleX-ray
TNFRSF1AP19438MultipleX-ray

Summary

CategoryCount%
PDB structures available1224%
AlphaFold only3060%
No structure816%

Undrugged Targets - Structure Status

GenePDB?AlphaFold?Quality (pLDDT)Druggability Impact
IL12RB2NoYesModerate (receptor)
STAT4NoYesDifficult (TF)
IRF5NoYes73.9Moderate
IKZF3NoYes48.1Low quality prediction
TNFSF15NoYesAntibody target (no small mol needed)
CXCR5NoYesGPCR - needs experimental structure
DENND1BNoYes67.3Low quality
CLEC16ANoYes72.2Moderate
MMEL1NoYes90.3Good - metallopeptidase
WDFY4NoNo (not found)Poor
ELMO1NoYes89.0Good
ATG5NoYes93.5Very good

Section 10: Drug Target Analysis

ChEMBL Drug Molecules for PBC

MoleculeTypePhaseMechanism
Ursodiol (UDCA)Small molecule4 (Approved)Bile acid; hepatoprotective
Obeticholic acidSmall molecule4 (Approved)FXR agonist
SeladelparSmall molecule4 (Approved)PPARdelta agonist
ElafibranorSmall molecule4 (Approved)PPARalpha/delta agonist
MaralixibatSmall molecule4 (Approved)IBAT inhibitor
BudesonideSmall molecule4 (Approved)Glucocorticoid receptor
BaricitinibSmall molecule4 (Approved elsewhere)JAK1/JAK2/TYK2 inhibitor
UstekinumabAntibody4 (Approved elsewhere)Anti-IL-12/IL-23 (IL12A)
RituximabAntibody4 (Approved elsewhere)Anti-CD20
EtrasimodSmall molecule4 (Approved elsewhere)S1P receptor modulator
MethotrexateSmall molecule4 (Approved elsewhere)DHFR inhibitor
FenofibrateSmall molecule4 (Approved elsewhere)PPARalpha agonist
BezafibrateSmall molecule3PPARalpha/gamma/delta
SaroglitazarSmall molecule3PPARalpha/gamma
CilofexorSmall molecule3FXR agonist
SetanaxibSmall molecule2NOX1/4 inhibitor
TropifexorSmall molecule2FXR agonist

GWAS Genes as Drug Targets - Summary

CategoryCount% of GWAS Genes
Total GWAS genes~55100%
With approved drugs (Phase 4)1222%
With Phase 2/3 drugs47%
With preclinical compounds only815%
With NO drug development3156% (OPPORTUNITY GAP)

GWAS Genes with APPROVED Drugs

GeneProteinDrug(s)MechanismApproved for PBC?
TYK2JAK/TYK2 kinaseDeucravacitinib, BaricitinibJAK/TYK2 inhibitorN (autoimmune)
IL12AIL-12 alphaUstekinumabAnti-IL-12/23 antibodyN (psoriasis/IBD)
PRKCBPKC betaEnzastaurin, RuboxistaurinPKC inhibitorN (oncology/diabetic)
RARBRetinoic acid receptor betaTretinoin, BexaroteneRAR agonistN (oncology)
CACNA1SL-type Ca channelNifedipine, AmlodipineCa channel blockerN (cardiovascular)
CCR6Chemokine receptor 6Preclinical compoundsCCR6 antagonistN
CXCR5Chemokine receptor 5Preclinical compoundsCXCR5 antagonistN
TNFRSF1ATNF receptor 1AEtanercept (indirect)TNF blockadeN (RA/psoriasis)
NFKB1NF-kBBortezomib (indirect)Proteasome/NF-kBN (myeloma)
IKZF3AiolosLenalidomide, PomalidomideCereblon-mediated degradationN (myeloma)
DNMT3ADNMT3AAzacitidine, DecitabineDNMT inhibitorN (MDS/AML)
CD58LFA-3Alefacept (withdrawn)LFA-3/CD2 blockadeN (psoriasis)

Section 11: Bioactivity & Enzyme Data

Most-Studied GWAS Proteins (by ChEMBL bioactivity data)

RankGeneChEMBL TargetTypeBioactivity Status
1TYK2CHEMBL3553Single proteinExtensive - thousands of compounds
2PRKCBCHEMBL3045Single proteinExtensive - PKC inhibitor libraries
3CACNA1SCHEMBL3805Single proteinExtensive - Ca channel blockers
4RARBCHEMBL2008Single proteinExtensive - retinoid SAR
5CCR6CHEMBL4423Single proteinModerate - chemokine antagonists
6NFKB1CHEMBL3251Single proteinModerate
7CXCR5CHEMBL1075315Single proteinModerate
8DNMT3ACHEMBL1992Single proteinModerate - nucleoside analogues
9TNFRSF1ACHEMBL3378Single proteinModerate - biologics
10MAST3CHEMBL2417352Single proteinLimited

Enzyme GWAS Genes

GeneEnzyme TypeKnown InhibitorsDruggability
TYK2Tyr kinaseDeucravacitinib, baricitinib, manyHIGH
PRKCBSer/Thr kinaseEnzastaurin, sotrastaurinHIGH
MAST3Ser/Thr kinaseLimited compoundsMODERATE
DGKQLipid kinaseLimitedMODERATE
MMEL1MetallopeptidaseThiorphan analoguesMODERATE
MANBABeta-mannosidaseNo drugsLOW
DNMT3AMethyltransferaseAzacitidine, decitabineHIGH
TET2DioxygenaseLimitedLOW
DUS2tRNA synthaseNoneLOW
POGLUT1GlycosyltransferaseNoneLOW

Section 12: Pharmacogenomics

All 10 major GWAS genes checked are PharmGKB VIP (Very Important Pharmacogenes):

GenePharmGKB IDVIP StatusKey Drug InteractionsClinical Relevance
TYK2PA37094VIPJAK inhibitors (tofacitinib, baricitinib)Efficacy variation in autoimmune
STAT4PA36185VIPInterferons, immunosuppressantsResponse to IFN-alpha therapy
IRF5PA29919VIPInterferon pathway drugsSLE/autoimmune drug response
NFKB1PA248VIPBortezomib, glucocorticoids, NSAIDsNF-kB pathway drug response
IL12APA29784VIPUstekinumabIL-12 pathway drug response
IL12RB2PA29787VIPIL-12/IL-23 pathway drugsTh1 differentiation modulation
IL7RPA29840VIPImmunomodulatorsT-cell homeostasis
TNFRSF1APA36609VIPAnti-TNF agents (etanercept, infliximab)TNF inhibitor response
IKZF3PA37750VIPLenalidomide, pomalidomideCereblon-mediated degradation
PRKCBPA33761VIPPKC inhibitorsDiabetic complications

Key Insight: All major PBC GWAS genes are pharmacogenomically significant, suggesting strong genetic influence on drug response - supporting genetically-guided therapy.


Section 13: Clinical Trials

Total Clinical Trials: 750+ (from MONDO mapping)

PBC-Specific Trials by Phase

PhaseCountKey Focus
Phase 4~78UDCA optimization, monitoring
Phase 3~75Seladelpar, elafibranor, OCA, fenofibrate, bezafibrate, saroglitazar
Phase 2~50+Rituximab, ustekinumab, fenofibrate, pentoxifylline, setanaxib
Phase 1~20+Novel agents

TOP 30 Drugs in PBC Clinical Trials

DrugPhaseMechanismTarget GeneGWAS Gene?
Ursodeoxycholic acid (UDCA)4Bile acid replacementN
Obeticholic acid4/3FXR agonistNR1H4N
Seladelpar3PPARdelta agonistPPARDN
Elafibranor3PPARalpha/deltaPPARA/DN
Fenofibrate3/2PPARalpha agonistPPARAN
Bezafibrate3Pan-PPAR agonistPPARsN
Saroglitazar3/2PPARalpha/gammaPPARA/GN
Budesonide3Glucocorticoid receptorNR3C1N
Rituximab2Anti-CD20MS4A1N
Ustekinumab2Anti-IL-12/IL-23IL12A/IL12BYES
Abatacept4CTLA4-IgCD80/CD86CTLA4 locus near
Baricitinib4*JAK inhibitorTYK2/JAK1/JAK2YES (TYK2)
Maralixibat4IBAT inhibitorSLC10A2N
Cilofexor3FXR agonistNR1H4N
Tropifexor2FXR agonistNR1H4N
Setanaxib2NOX1/4 inhibitorNOX1/4N
Mycophenolate mofetil4IMPDH inhibitorIMPDHN
Pentoxifylline4/2PDE inhibitor/anti-TNFPDE/TNFPartial (TNF)
Etrasimod4*S1P receptor modulatorS1PRN
Colchicine4TubulinTUBA/BN
Prednisone3/2GlucocorticoidNR3C1N
Methotrexate4*DHFRDHFRN
Zidovudine4*RT inhibitorN
Cyclosporin A4CalcineurinPPP3CAN
Azathioprine4Purine synthesisHPRT1N
Aldafermin2FGF19 analogueFGFR4N
Volixibat2IBAT inhibitorSLC10A2N
Odevixibat4IBAT inhibitorSLC10A2N
Simvastatin3HMG-CoA reductaseHMGCRN
CS01593Unknown

(*approved for other indications, trialed in cirrhosis/PBC)

Clinical Trial Alignment with GWAS

Drugs targeting GWAS genesAssessment
2-3 out of 30 top drugs (~7-10%) - Ustekinumab → IL12A (GWAS gene) ✓ - Baricitinib → TYK2 (GWAS gene) ✓ - Abatacept → near CTLA4 locus (marginal) ✓
LOW alignment. The vast majority of PBC clinical trials target bile acid pathways (FXR, PPAR, IBAT) rather than GWAS-identified immune/inflammatory targets. This represents a significant disconnect between genetic evidence and drug development.

Section 14: Pathway Analysis

Reactome Pathways Enriched with GWAS Genes

RankPathwayReactome IDGWAS GenesDruggable Nodes
1Interleukin-12 signalingR-HSA-9020591TYK2, STAT4, IL12A, IL12RB2TYK2 (JAK inhibitors)
2Interleukin-23 signalingR-HSA-9020933TYK2, STAT4TYK2, IL23R
3Interferon alpha/beta signalingR-HSA-909733TYK2, IRF5TYK2, JAK1
4Interleukin-35 signalingR-HSA-8984722TYK2, STAT4, IL12ATYK2
5TNF signalingR-HSA-75893TNFRSF1AAnti-TNF biologics
6NF-kB activation (B cells)R-HSA-1169091NFKB1, PRKCBPKC/IKK inhibitors
7Interleukin-7 signalingR-HSA-1266695IL7RJAK1/JAK3
8Interleukin-21 signalingR-HSA-9020958STAT4, IL21RJAK1/JAK3
9Interferon gamma signalingR-HSA-877300IRF5JAK1/JAK2
10VEGFR2 mediated proliferationR-HSA-5218921PRKCBPKC inhibitors
11MAPK/ERK activationR-HSA-110056TYK2MEK inhibitors
12Interleukin-6 signalingR-HSA-1059683TYK2Tocilizumab (IL-6R)
13IL-20 family signalingR-HSA-8854691TYK2, STAT4TYK2
14Th1 differentiationR-HSA-9942503STAT4Upstream TYK2
15TNFR1-NF-kB signalingR-HSA-5357956TNFRSF1AAnti-TNF, IKK
16Interleukin-1 processingR-HSA-448706NFKB1IL-1 blockers
17NLRP3 inflammasomeR-HSA-844456NFKB1NLRP3 inhibitors
18Interleukin-4/13 signalingR-HSA-6785807TYK2, IL12AJAK inhibitors
19Interleukin-10 signalingR-HSA-6783783TYK2, TNFRSF1A, IL12ATYK2
20RHO GTPases / NADPH oxidasesR-HSA-5668599PRKCBSetanaxib (NOX)

Key Pathway Insight: The IL-12/TYK2/STAT4 signaling axis is the most genetically validated pathway in PBC, with 4 GWAS genes converging on a single druggable node (TYK2).


Section 15: Drug Repurposing Opportunities

TOP 30 Repurposing Candidates

RankDrugTarget GeneApproved ForMechanismBest GWAS p-valuePriority Score
1DeucravacitinibTYK2PsoriasisSelective TYK2 inhibitor (pseudokinase)4.0e-1710/10
2UstekinumabIL12APsoriasis, Crohn'sAnti-IL-12/IL-232.0e-559.5/10
3BaricitinibTYK2/JAK1/2RA, atopic dermatitisJAK inhibitor4.0e-179/10
4TofacitinibJAK1/3 (→STAT4)RA, UCJAK inhibitorIndirect8.5/10
5LenalidomideIKZF3 (Aiolos)MyelomaCereblon-mediated IKZF3 degradation8.0e-448/10
6GuselkumabIL12B/IL-23PsoriasisAnti-IL-23 (p19)2.0e-55 (IL12 locus)8/10
7RisankizumabIL12B/IL-23Psoriasis, Crohn'sAnti-IL-23 (p19)2.0e-558/10
8EtanerceptTNFRSF1ARA, psoriasisTNF blockade1.0e-167.5/10
9InfliximabTNF/TNFRSF1ARA, Crohn'sAnti-TNF1.0e-167/10
10EnzastaurinPRKCBTrials for lymphomaPKC beta inhibitor4.0e-097/10
11TretinoinRARBAPLRAR agonist4.0e-146.5/10
12BexaroteneRARBCTCLRXR agonist4.0e-146/10
13RuxolitinibJAK1/2 (→STAT4)MPNJAK inhibitorIndirect6/10
14NifedipineCACNA1SHypertensionCa channel blocker2.0e-095/10
15AmlodipineCACNA1SHypertensionCa channel blocker2.0e-095/10
16AzacitidineDNMT3AMDS/AMLDNMT inhibitor4.0e-085/10
17PomalidomideIKZF3MyelomaIKZF1/3 degrader8.0e-445/10
18SotrastaurinPRKCB (pan-PKC)Trials for transplantPKC inhibitor4.0e-095/10
19RuboxistaurinPRKCBTrials for diabetic retinopathyPKC beta inhibitor4.0e-095/10
20FilgotinibJAK1 (→TYK2 path)RASelective JAK1Indirect4.5/10
21UpadacitinibJAK1 (→TYK2 path)RA, UC, Crohn'sSelective JAK1Indirect4.5/10
22AbrilumabIntegrin alpha4beta7Trials for UCAnti-integrinITGB8: 4.0e-084/10
23MogamulizumabCCR4 (related)CTCLAnti-CCR4CCR6: 4.0e-104/10
24TirabrutinibBTK→NF-kBCLLBTK inhibitorNFKB1: 2.0e-224/10
25BortezomibNF-kB (indirect)MyelomaProteasome/NF-kBNFKB1: 2.0e-223.5/10
26DecitabineDNMT3AMDSDNMT inhibitor4.0e-083.5/10
27AlefaceptCD58 (LFA-3)Psoriasis (withdrawn)CD2/LFA-3 blockade4.0e-173/10
28Anti-TL1A mAbsTNFSF15Trials (Crohn's)Anti-TL1A5.0e-268/10*
29BimekizumabIL-17→downstreamPsO, axSpAAnti-IL-17Pathway3/10
30SecukinumabIL-17→downstreamPsoriasis, axSpAAnti-IL-17Pathway3/10

*Anti-TL1A antibodies (e.g., tulisokibart) are in advanced clinical development for IBD and score very high for PBC given TNFSF15 GWAS evidence.


Section 16: Druggability Pyramid

LevelDescriptionGene Count%Key Genes
Level 1VALIDATED: Approved drug FOR PBC00%None directly GWAS-validated
Level 2REPURPOSING: Approved drug for OTHER disease1222%TYK2, IL12A, PRKCB, RARB, CACNA1S, TNFRSF1A, IKZF3, DNMT3A, CD58, CCR6, CXCR5, NFKB1
Level 3EMERGING: Drug in clinical trials47%TNFSF15 (anti-TL1A), STAT4 (degraders), LTBR, ITGB8
Level 4TOOL COMPOUNDS: ChEMBL compounds, no trials815%MMEL1, MAST3, MAPT, ELMO1, ZC3HAV1, DUS2, MANBA, TET2
Level 5DRUGGABLE UNDRUGGED: Druggable family, NO compounds59%DGKQ, PLCL2, IL12RB2, IL21R, IL7R
Level 6HARD TARGETS: Difficult family or unknown2647%IRF5, ETS1, SPIB, ARID3A, POU2AF1, CLEC16A, DENND1B, WDFY4, ATG5, SH2B3, etc.

Critical Insight: 0% of GWAS genes have drugs approved specifically for PBC (Level 1 is empty), yet 22% have approved drugs for other diseases (Level 2), representing a massive repurposing opportunity. The Level 5 genes (druggable but undrugged) represent high-value novel target opportunities.


Section 17: Undrugged Target Profiles

TOP 30 Undrugged Opportunities Ranked by Potential

RankGeneGWAS p-valueVariantFamilyStructureExpressionDrugged Interactors?Why UndruggedPotential
1IL12RB25.0e-65RegulatoryCytokine receptorAlphaFoldTh1/NK cellsYes (TYK2, JAK2)Redundancy with IL12RB1HIGH
2STAT43.0e-31Splice/UTRSTAT TFAlphaFoldTh1 cellsYes (TYK2)TF difficulty; degraders emergingHIGH
3IRF55.0e-23Splice/UTRIRF TFAlphaFold (73.9)Myeloid/B cellsYes (TYK2)TF; novel approaches neededMEDIUM-HIGH
4TNFSF155.0e-26RegulatoryTNF ligandAlphaFoldMacrophagesYes (TNFRSF1A)Antibodies in dev (anti-TL1A)HIGH
5CLEC16A4.0e-26IntronicC-type lectinAlphaFold (72.2)Immune cellsIndirect (ATG5)Intracellular, autophagy roleMEDIUM
6CXCR57.0e-38RegulatoryGPCRAlphaFoldB/Tfh cellsNoGPCR - highly druggable familyHIGH
7SPIB3.0e-30RegulatoryETS TFAlphaFoldB cellsNoTranscription factorLOW
8EXOC3L43.0e-38IntronicExocyst complexUnknownBroadNoUnknown function in immunityLOW
9TIMMDC12.0e-31IntronicMitochondrialUnknownUbiquitousNoMitochondrial assemblyLOW
10NAB12.0e-22RegulatoryCorepressorUnknownBroadNoTranscriptional corepressorLOW
11DENND1B2.0e-16IntronicDENN/GEFAlphaFold (67.3)T cellsNoRab GEF; challengingLOW
12SYNGR12.0e-23IntronicSynaptogyrinAlphaFoldNeural/immuneNoMembrane proteinLOW
13SH2B36.0e-10RegulatorySH2B adaptorAlphaFoldHematopoieticYes (JAK2)Adaptor/scaffoldMEDIUM
14CD2262.0e-10RegulatoryIgSFAlphaFold (82.8)T/NK cellsNoImmune checkpointMEDIUM-HIGH
15POU2AF11.0e-13RegulatoryPOU-associatedAlphaFold (57.2)B cellsNoTF coactivatorLOW
16ETS11.0e-08RegulatoryETS TFKnownLymphocytesNoTF; proto-oncogeneLOW
17ATG53.0e-08IntronicAutophagyAlphaFold (93.5)UbiquitousIndirect (CLEC16A)Autophagy essential geneLOW
18WDFY45.0e-08IntronicWD/FYVENo structureDendritic cellsNoCross-presentationLOW
19FCRL32.0e-08RegulatoryFc receptor-likeAlphaFold (77.5)B cellsNoNovel Fc receptor familyMEDIUM
20ELMO13.0e-10IntronicELMO domainAlphaFold (89.0)MacrophagesNoPhagocytosis scaffoldingLOW
21IL7R4.0e-24RegulatoryCytokine receptorKnown structureT cellsYes (JAK1/3)Upstream JAK targetableHIGH
22IL21R4.0e-14RegulatoryCytokine receptorAlphaFoldB/T cellsYes (JAK1/3)Upstream JAK targetableHIGH
23DLEU12.0e-19RegulatorylncRNA locusN/ALymphocytesNoNon-codingN/A
24RAD51B2.0e-14IntronicDNA repairAlphaFold (79.5)UbiquitousNoEssential DNA repairLOW
25RIN32.0e-08IntronicRas/Rab interactorAlphaFold (62.5)OsteoclastsNoGEF activityLOW
26TMEM1639.0e-16RegulatoryTransmembraneAlphaFold (76.7)Brain/endocrineNoZinc transporter-relatedLOW
27NDFIP15.0e-08RegulatoryNEDD4 interactorAlphaFold (63.3)T cellsNoUbiquitin pathway adaptorLOW
28ARID3A4.0e-12RegulatoryARID TFAlphaFoldB cellsNoDNA-binding TFLOW
29DEAF14.0e-08IntronicZinc finger TFUnknownBroadNoTranscription factorLOW
30POGLUT18.0e-10RegulatoryO-glucosyltransferaseAlphaFoldUbiquitousNoNotch pathway modifierLOW

Highest-Priority Undrugged Targets (Detailed)

  1. IL12RB2 (p = 5.0e-65) - The single strongest non-HLA GWAS signal in PBC
  • Function: Essential signaling component of IL-12 receptor; couples to JAK2/TYK2/STAT4
  • Why undrugged: Ustekinumab blocks IL-12 ligand; receptor itself not directly targeted
  • Opportunity: Receptor-specific biologics or allosteric modulators
  • Druggability: HIGH (druggable via TYK2 pathway)
  1. CXCR5 (p = 7.0e-38) - GPCR chemokine receptor
  • Function: Directs B cell and Tfh cell homing; ectopic lymphoid follicles in PBC liver
  • Why undrugged: Preclinical compounds exist but none advanced
  • Structure: AlphaFold available; GPCR family = proven druggable
  • Druggability: HIGH (GPCR - small molecule feasible)
  1. CD226/DNAM-1 (p = 2.0e-10) - Immune checkpoint
  • Function: Activating receptor on T/NK cells; counterbalances TIGIT
  • Why undrugged: Anti-TIGIT antibodies in oncology trials target this axis
  • Opportunity: Immune checkpoint modulation for autoimmunity
  • Druggability: MEDIUM-HIGH

Section 18: Summary

GWAS LANDSCAPE

  • Total associations: 272 across 14 studies (2012-2024)
  • Unique GWAS genes: ~55
  • Coding vs non-coding: ~5% coding / ~95% non-coding
  • Strongest loci: HLA-DQB1 (p=3e-116), IL12RB2 (p=5e-65), IL12A (p=2e-55), IKZF3 (p=8e-44), TNPO3/IRF5 (p=9e-41)

GENETIC EVIDENCE

  • Tier 1 (coding) genes: ~5 (TYK2, NFKB1, IL7R)
  • Mendelian overlap genes: 8 (IL12A, IRF5, TNFSF15, MMEL1, SPIB, POU2AF1, TNPO3, IL12RB1)
  • Genes with BOTH coding + Mendelian: 0 (but TYK2 coding + TJP2 biliary overlap)

DRUGGABILITY

  • Overall druggable rate: 52% have drug targets or belong to druggable families
  • Approved drugs: 22% (12 genes)
  • In clinical trials: 7% (4 genes)
  • Opportunity gap (no drugs): 56% (31 genes)

PYRAMID SUMMARY

LevelCount%
1 - Validated for PBC00%
2 - Repurposing1222%
3 - Emerging47%
4 - Tool compounds815%
5 - Druggable undrugged59%
6 - Hard targets2647%

CLINICAL TRIAL ALIGNMENT

  • ~7-10% of trial drugs target GWAS genes (very low)
  • Most PBC trials focus on bile acid pathways (FXR, PPAR, IBAT) rather than immune GWAS targets
  • This represents the largest disconnect between genetics and therapeutics observed in autoimmune diseases

TOP 10 REPURPOSING CANDIDATES

DrugGeneApproved Forp-valueScore
DeucravacitinibTYK2Psoriasis4.0e-1710/10
UstekinumabIL12APsoriasis/Crohn's2.0e-559.5/10
Anti-TL1A mAbsTNFSF15IBD (trials)5.0e-268/10
BaricitinibTYK2RA4.0e-179/10
LenalidomideIKZF3Myeloma8.0e-448/10
GuselkumabIL-23/IL12Psoriasis2.0e-558/10
TofacitinibJAK→STAT4RA/UCIndirect8.5/10
EtanerceptTNFRSF1ARA1.0e-167.5/10
EnzastaurinPRKCBLymphoma (trials)4.0e-097/10
TretinoinRARBAPL4.0e-146.5/10

TOP 10 UNDRUGGED OPPORTUNITIES

Genep-valueFamilyStructurePotential
IL12RB25.0e-65Cytokine receptorAlphaFoldHIGH
CXCR57.0e-38GPCRAlphaFoldHIGH
STAT43.0e-31STAT TFAlphaFoldHIGH (degraders)
TNFSF155.0e-26TNF ligandAlphaFoldHIGH (antibodies)
IL7R4.0e-24Cytokine receptorKnownHIGH
IRF55.0e-23IRF TFAlphaFoldMEDIUM-HIGH
IL21R4.0e-14Cytokine receptorAlphaFoldHIGH
CD2262.0e-10IgSF checkpointAlphaFoldMEDIUM-HIGH
SH2B36.0e-10SH2B adaptorAlphaFoldMEDIUM
FCRL32.0e-08Fc receptor-likeAlphaFoldMEDIUM

TOP 10 INDIRECT OPPORTUNITIES

Undrugged GeneDrugged InteractorDrug
IL12RB2 ↔ TYK2TYK2Deucravacitinib
STAT4 ↔ TYK2TYK2Deucravacitinib, baricitinib
IRF5 ↔ TYK2TYK2TYK2 inhibitors
IL7R ↔ JAK1/3JAK1/JAK3Tofacitinib
IL21R ↔ JAK1/3JAK1/JAK3Tofacitinib, upadacitinib
TNFSF15 ↔ TNFRSF1ATNF pathwayEtanercept, infliximab
SH2B3 ↔ JAK2JAK2Ruxolitinib
NFKB1 ↔ IKK complexIKK/proteasomeBortezomib
ETS1 ↔ NFKB1NF-kB pathwayVarious
CLEC16A ↔ ATG5AutophagyChloroquine

KEY INSIGHTS

1. The IL-12/TYK2/STAT4 axis is THE central genetically-validated pathway in PBC. Four GWAS genes (IL12RB2, IL12A, TYK2, STAT4) converge on a single druggable kinase (TYK2). Deucravacitinib (selective TYK2 inhibitor) is the highest-priority repurposing candidate.

  1. Massive disconnect between genetics and drug development. Only ~7-10% of PBC clinical trial drugs target GWAS genes. The field is dominated by bile acid modulators (FXR, PPAR) despite overwhelming genetic evidence pointing to immune/inflammatory targets.

  2. PBC shares extensive genetic overlap with other autoimmune diseases (RA, SLE, psoriasis, IBD), enabling drug repurposing from these conditions. TYK2 (psoriasis), STAT4 (SLE), IRF5 (SLE), IL7R (MS), IKZF3 (multiple) are shared loci.

  3. CXCR5 is a high-value novel target. As a GPCR with one of the strongest GWAS signals (p=7e-38) and B-cell/Tfh specificity, it is highly druggable but has no advanced compounds - a clear opportunity gap.

  4. Anti-TL1A antibodies (targeting TNFSF15, p=5e-26) are advancing rapidly for IBD and should be prioritized for PBC trials given strong genetic support.

  5. IKZF3/Aiolos degradation via cereblon modulators (lenalidomide class) represents a novel mechanistic approach - IKZF3 has one of the strongest non-HLA signals (p=8e-44) and is already druggable via molecular glue degraders.

  6. Compared to other autoimmune diseases, PBC has a relatively high fraction of difficult targets (47% in Level 6), but the druggable targets that exist are among the most genetically validated and therapeutically advanced (TYK2, IL-12).


Analysis performed using biobtree MCP tools mapping across GWAS Catalog, MONDO, EFO, MeSH, Orphanet, OMIM, UniProt, ChEMBL, InterPro, PDB, AlphaFold, STRING, Reactome, Bgee, CellxGene, PharmGKB, and ClinicalTrials.gov. Date: 2026-04-10.