Multiple cutaneous and mucosal venous malformations

Summary

Multiple cutaneous and mucosal venous malformations (MONDO:0010842) is a disease caused by TEK (GenCC Definitive), with 1 cohort gene.

At a glance

• Prevalence: (Worldwide) [Orphanet-validated]
• Causal gene: TEK (GenCC Definitive)
• Cohort genes: 1
• ClinVar variants: 134

Clinical features

Epidemiology

Prevalence records

2 prevalence record(s), Orphanet:

Type	Class	Value	Geography	Validation
Cases/families		18	Worldwide	Validated
Point prevalence	<1 / 1 000 000		Europe	Not yet validated

Identifiers

Disease identifiers

Field	Value
Canonical name	multiple cutaneous and mucosal venous malformations
Mondo ID	MONDO:0010842
MeSH	C563977
OMIM	600195
Orphanet	2451
DOID	DOID:0050792
SNOMED CT	699301008
UMLS	C1838437
MedGen	325026
GARD	0016600
Is cancer (heuristic)	no

Also known as: cutaneous and mucosal venous malformation · VENOUS malformations, multiple cutaneous and mucosal · VMCM

Data availability: 134 ClinVar variants · 5 GenCC gene-disease records.

Disease family

Classification path: disease › human disease › disease by etiologic mechanism › disease of genetic or genomic mechanism › hereditary disease › autosomal genetic disease › autosomal dominant disease › multiple cutaneous and mucosal venous malformations

Related subtypes (191): autosomal dominant polycystic liver disease, cerebral arteriopathy, autosomal dominant, with subcortical infarcts and leukoencephalopathy, type 1, tuberous sclerosis, Treacher-Collins syndrome, hereditary breast ovarian cancer syndrome, autosomal dominant polycystic kidney disease, Lynch syndrome, branchio-oto-renal syndrome, autosomal dominant Aarskog syndrome, acroosteolysis dominant type, ADULT syndrome, autosomal dominant Alport syndrome, amelogenesis imperfecta type 1B, Townes-Brocks syndrome, nevoid basal cell carcinoma syndrome, blepharophimosis, ptosis, and epicanthus inversus syndrome, autosomal dominant brachyolmia, branchiooculofacial syndrome, pheochromocytoma/paraganglioma syndrome 4, cataract-aberrant oral frenula-growth delay syndrome, cherubism, autosomal dominant chondrodysplasia punctata, autosomal dominant popliteal pterygium syndrome, blepharocheilodontic syndrome, cochleosaccular degeneration-cataract syndrome, renal coloboma syndrome, Beare-Stevenson cutis gyrata syndrome, autosomal dominant vibratory urticaria, neurohypophyseal diabetes insipidus, autosomal dominant Kenny-Caffey syndrome, Rapp-Hodgkin syndrome, Ehlers-Danlos syndrome, classic type, autosomal dominant Ehlers-Danlos syndrome, vascular type, multiple endocrine neoplasia type 1, Coffin-Siris syndrome 1, isolated congenital adermatoglyphia, Flynn-Aird syndrome, Frasier syndrome, hand-foot-genital syndrome, Holt-Oram syndrome, hyperkeratosis-hyperpigmentation syndrome, autosomal dominant ichthyosis vulgaris, hyper-IgE recurrent infection syndrome 1, autosomal dominant, autosomal dominant keratitis, autosomal dominant keratitis-ichthyosis-hearing loss syndrome, LADD syndrome, trichorhinophalangeal syndrome type II, Noonan syndrome with multiple lentigines, microcephaly with or without chorioretinopathy, lymphedema, or intellectual disability, Marfan syndrome, melanoma, cutaneous malignant, susceptibility to, 2, autosomal dominant primary microcephaly, autosomal dominant progressive external ophthalmoplegia, monilethrix, Muir-Torre syndrome, autosomal dominant myoglobinuria, autosomal dominant centronuclear myopathy, nail-patella syndrome, multiple endocrine neoplasia type 2B, autosomal dominant omodysplasia, pheochromocytoma/paraganglioma syndrome 1, Pelger-Huet anomaly, multiple endocrine neoplasia type 2A, piebaldism, autosomal dominant medullary cystic kidney disease with or without hyperuricemia, generalized juvenile polyposis/juvenile polyposis coli, juvenile polyposis/hereditary hemorrhagic telangiectasia syndrome, Peutz-Jeghers syndrome, contractures, pterygia, and spondylocarpotarsal fusion syndrome 1A, autosomal dominant distal renal tubular acidosis, retinoschisis, autosomal dominant, autosomal dominant Robinow syndrome, scapuloperoneal spinal muscular atrophy, autosomal dominant, autosomal dominant sideroblastic anemia, spondyloepiphyseal dysplasia tarda, autosomal dominant, proximal symphalangism, calcaneonavicular coalition, thanatophoric dysplasia type 1, trichorhinophalangeal syndrome type I, Muckle-Wells syndrome, autosomal dominant hypophosphatemic rickets, von Hippel-Lindau disease, Denys-Drash syndrome, autosomal dominant severe congenital neutropenia, Costello syndrome, EEC syndrome, diffuse nonepidermolytic palmoplantar keratoderma, Timothy syndrome, pheochromocytoma/paraganglioma syndrome 2, spondyloepimetaphyseal dysplasia with multiple dislocations, Brooke-Spiegler syndrome, macrocephaly-autism syndrome, pheochromocytoma/paraganglioma syndrome 3, Duane-radial ray syndrome, PCWH syndrome, heart-hand syndrome, Slovenian type, congenital stationary night blindness autosomal dominant 3, mandibulofacial dysostosis-microcephaly syndrome, multiple endocrine neoplasia type 4, juvenile cataract-microcornea-renal glucosuria syndrome, Crouzon syndrome-acanthosis nigricans syndrome, Birk-Barel syndrome, thrombophilia due to protein S deficiency, autosomal dominant, dyskeratosis congenita, autosomal dominant 2, dyskeratosis congenita, autosomal dominant 3, colorectal cancer, hereditary nonpolyposis, type 6, colorectal cancer, hereditary nonpolyposis, type 7, brain small vessel disease 2A, autosomal dominant, intellectual disability, autosomal dominant 14, intellectual disability, autosomal dominant 15, intellectual disability, autosomal dominant 16, hypopigmentation-punctate palmoplantar keratoderma syndrome, intellectual disability-facial dysmorphism syndrome due to SETD5 haploinsufficiency, postaxial polydactyly-anterior pituitary anomalies-facial dysmorphism syndrome, intellectual developmental disorder with microcephaly and with or without ocular malformations or hypogonadotropic hypogonadism, intellectual disability, autosomal dominant 29, intellectual disability, autosomal dominant 30, Houge-Janssens syndrome 2, severe achondroplasia-developmental delay-acanthosis nigricans syndrome, dyskeratosis congenita, autosomal dominant 6, epidermolysis bullosa simplex 6, generalized, with scarring and hair loss, autosomal dominant complex spastic paraplegia, early-onset autosomal dominant Alzheimer disease, muscular dystrophy, limb-girdle, autosomal dominant, Feingold syndrome, Carney complex, neuronopathy, distal hereditary motor, autosomal dominant, autosomal dominant coarctation of aorta, autosomal dominant spondylocostal dysostosis, autosomal dominant hypohidrotic ectodermal dysplasia, Cowden disease, autosomal dominant distal myopathy, autosomal dominant rhegmatogenous retinal detachment, palmoplantar keratoderma-spastic paralysis syndrome, Alagille syndrome due to a JAG1 point mutation, PTEN hamartoma tumor syndrome, gastric adenocarcinoma and proximal polyposis of the stomach, autosomal dominant proximal renal tubular acidosis, autosomal dominant spastic ataxia, Waardenburg syndrome, hereditary retinoblastoma, autosomal dominant hypocalcemia, Li-Fraumeni syndrome, Loeys-Dietz syndrome, hereditary hemorrhagic telangiectasia, hereditary inclusion body myopathy-joint contractures-ophthalmoplegia syndrome, microcephalic osteodysplastic dysplasia, Saul-Wilson type, autosomal dominant intermediate Charcot-Marie-Tooth disease, autosomal dominant cutis laxa, autosomal dominant nonsyndromic hearing loss, autosomal dominant optic atrophy, autosomal dominant Emery-Dreifuss muscular dystrophy, autosomal dominant cerebellar ataxia, autosomal dominant osteopetrosis, autosomal dominant epidermolytic ichthyosis, ventricular arrhythmias due to cardiac ryanodine receptor calcium release deficiency syndrome, distal arthrogryposis type 2B1, neurofibromatosis, autosomal dominant cataract, arthrogryposis, distal, type 2B2, arthrogryposis, distal, type 2B3, Charcot-Marie-Tooth disease, demyelinating, type 1G, Delpire-McNeill syndrome, LAMA5-related multisystemic syndrome, autosomal dominant oculocutaneous albinism, Charcot-Marie-tooth disease, axonal, type 2DD, Pilarowski-Bjornsson syndrome, intellectual disability, autosomal dominant, fatty acyl-CoA reductase 1 upregulation, GUCY2D-related dominant retinopathy, RPE65-related dominant retinopathy, autosomal dominant titinopathy, NOG-related symphalangism spectrum disorder, ALPL-related autosomal dominant hypophosphatasia, MYH10-related neurodevelopmental disorder with congenital anomalies, spastic paraplegia 30A, autosomal dominant, TMEM127-related tumor predisposition, MAX-related tumor predisposition, BMPR1A-related juvenile polyposis syndrome, RP1-related dominant retinopathy, Birt-Hogg-Dube syndrome, inclusion body myopathy and brain white matter abnormalities, KINSSHIP syndrome, autosomal dominant nebulin-related myopathy, IMPG1-related dominant retinopathy, PROM1-related dominant retinopathy, PURA-related severe neonatal hypotonia-seizures-encephalopathy syndrome, ALG8-related autosomal dominant polycystic kidney and/or liver disease, NOTCH1-related AOS spectrum disorder, FLNB-associated autosomal dominant filamin related bone disorder, familial antiphospholipid syndrome

Genetics & variants

GWAS landscape

No GWAS associations recorded — common-variant (GWAS) studies don’t cover this disease (typical for Mendelian / rare diseases). See the curated gene cohort and Mendelian overlap below.

Variant details and genetic-evidence tiers

ClinVar germline variants

134 retrieved; paginated sample, class counts are floors:

48 benign, 44 uncertain significance, 10 conflicting classifications of pathogenicity, 10 benign/likely benign, 8 pathogenic, 7 likely pathogenic, 5 pathogenic/likely pathogenic, 1 not provided, 1 likely benign

ClinVar	Variant (HGVS)	Gene	Classification	Review
1691345	NM_000459.5(TEK):c.2689T>A (p.Tyr897Asn)	TEK	Pathogenic/Likely pathogenic	criteria provided, multiple submitters, no conflicts
2664276	NM_000459.5(TEK):c.3323_3324del (p.Leu1107_Tyr1108insTer)	TEK	Pathogenic	criteria provided, single submitter
30053	NM_000459.5(TEK):c.2690A>G (p.Tyr897Cys)	TEK	Pathogenic	criteria provided, multiple submitters, no conflicts
30054	NM_000459.5(TEK):c.2744G>A (p.Arg915His)	TEK	Pathogenic/Likely pathogenic	criteria provided, multiple submitters, no conflicts
3340431	NM_000459.5(TEK):c.3338dup (p.Tyr1113Ter)	TEK	Pathogenic	criteria provided, single submitter
3340457	NM_000459.5(TEK):c.3324T>G (p.Tyr1108Ter)	TEK	Pathogenic	criteria provided, single submitter
3780702	NM_000459.5(TEK):c.1552C>T (p.Gln518Ter)	TEK	Pathogenic/Likely pathogenic	criteria provided, multiple submitters, no conflicts
9293	NM_000459.5(TEK):c.2545C>T (p.Arg849Trp)	TEK	Pathogenic	criteria provided, multiple submitters, no conflicts
981227	NM_000459.5(TEK):c.2743C>T (p.Arg915Cys)	TEK	Pathogenic/Likely pathogenic	criteria provided, multiple submitters, no conflicts
981228	NM_000459.5(TEK):c.2752C>T (p.Arg918Cys)	TEK	Pathogenic/Likely pathogenic	criteria provided, multiple submitters, no conflicts
981230	NM_000459.5(TEK):c.3295C>T (p.Arg1099Ter)	TEK	Pathogenic	criteria provided, multiple submitters, no conflicts
981231	NM_000459.5(TEK):c.3324T>A (p.Tyr1108Ter)	TEK	Pathogenic	criteria provided, single submitter
981232	NM_000459.5(TEK):c.3343G>T (p.Gly1115Ter)	TEK	Pathogenic	criteria provided, single submitter
3238631	NM_000459.5(TEK):c.3323_3324insCGTGAATACCACGCTTTATGAGAAGTAGTA (p.Tyr1108_Glu1109insValAsnThrThrLeuTyrGluLysTer)	TEK	Likely pathogenic	criteria provided, single submitter
3238638	NM_000459.5(TEK):c.2750G>T (p.Ser917Ile)	TEK	Likely pathogenic	criteria provided, single submitter
3376501	NM_000459.5(TEK):c.2491G>T (p.Gly831Trp)	TEK	Likely pathogenic	criteria provided, single submitter
3780703	NM_000459.5(TEK):c.578del (p.Tyr193fs)	TEK	Likely pathogenic	criteria provided, single submitter
4279763	NM_000459.5(TEK):c.3324_3334del (p.Glu1109fs)	TEK	Likely pathogenic	criteria provided, single submitter
917490	NM_000459.5(TEK):c.2678A>T (p.Glu893Val)	TEK	Likely pathogenic	no assertion criteria provided
9294	NM_000459.5(TEK):c.2690A>C (p.Tyr897Ser)	TEK	Likely pathogenic	criteria provided, single submitter
366393	NM_000459.5(TEK):c.309A>C (p.Glu103Asp)	TEK	Conflicting classifications of pathogenicity	criteria provided, conflicting classifications
366423	NM_000459.5(TEK):c.1387A>G (p.Ile463Val)	TEK	Conflicting classifications of pathogenicity	criteria provided, conflicting classifications
366424	NM_000459.5(TEK):c.1390A>C (p.Asn464His)	TEK	Conflicting classifications of pathogenicity	criteria provided, conflicting classifications
431835	NM_000459.5(TEK):c.2078C>T (p.Thr693Ile)	TEK	Conflicting classifications of pathogenicity	criteria provided, conflicting classifications
913743	NM_000459.5(TEK):c.267G>T (p.Lys89Asn)	TEK	Conflicting classifications of pathogenicity	criteria provided, conflicting classifications
914142	NM_000459.5(TEK):c.484A>T (p.Ile162Phe)	TEK	Conflicting classifications of pathogenicity	criteria provided, conflicting classifications
914145	NM_000459.5(TEK):c.882G>C (p.Lys294Asn)	TEK	Conflicting classifications of pathogenicity	criteria provided, conflicting classifications
914283	NM_000459.5(TEK):c.1507A>G (p.Thr503Ala)	TEK	Conflicting classifications of pathogenicity	criteria provided, conflicting classifications
930496	NM_000459.5(TEK):c.2773G>A (p.Ala925Thr)	TEK	Conflicting classifications of pathogenicity	criteria provided, conflicting classifications
976620	NM_000459.5(TEK):c.2546G>A (p.Arg849Gln)	TEK	Conflicting classifications of pathogenicity	criteria provided, conflicting classifications

Genes & proteins

Mendelian disease overlap and somatic drivers

GenCC: 9 · Orphanet: 4 · OMIM-shared: 0 · Dual-evidence (GWAS+Mendelian): 0

GenCC gene–disease validity (cohort genes)

the Disease column is the GenCC-asserted condition — a cohort gene’s strongest validity may be for a related predisposition syndrome.

Gene	Classification	Inheritance	Disease	Records
TEK	Definitive	Autosomal dominant	multiple cutaneous and mucosal venous malformations	9

Orphanet rare-disease linkage (cohort genes)

Gene	Orphanet ID	Rare disease
TEK	Orphanet:1059	Blue rubber bleb nevus
TEK	Orphanet:2451	Mucocutaneous venous malformations
TEK	Orphanet:714806	Multifocal sporadic venous malformation
TEK	Orphanet:98976	Congenital glaucoma

Cohort genes → proteins

1 cohort genes, 1 distinct canonical proteins.

Evidence partition

Subset	Genes
multi_evidence	1

Cohort genes (full)

Symbol	HGNC	Ensembl	UniProt	Name	Evidence
TEK	HGNC:11724	ENSG00000120156	Q02763	Angiopoietin-1 receptor	gencc,clinvar

Cohort function summary

Lead sentence per gene, UniProt-curated.

Symbol	Protein name	Function (lead sentence)
TEK	Angiopoietin-1 receptor	Tyrosine-protein kinase that acts as a cell-surface receptor for ANGPT1, ANGPT2 and ANGPT4 and regulates angiogenesis, endothelial cell survival, proliferation, migration, adhesion and cell spreading, reorganization of the actin cytoskelet…

Protein-family classification

Druggable: 1 · Difficult: 0 · Unknown: 0 · Druggable fraction: 1.0

Family distribution

Cohort families vs a genome-wide background (hypergeometric, BH-FDR; fold = observed/expected). Counts kept; sorted by enrichment, so the catch-all Other/Unknown bucket no longer leads.

Family	Genes	Fold	FDR
Kinase	1	27.7×	0.036

Per-gene assignment

Symbol	Family	Druggable?	EC	InterPro (top 3)
TEK	Kinase	yes	2.7.10.1	Prot_kinase_dom, EGF, Ser-Thr/Tyr_kinase_cat_dom

Expression context

Cohort genes with no expression data: 0.

1 cohort gene are a single-cell marker in ≥1 SCXA experiment.

Breadth distribution (Bgee present_calls)

Bucket	Genes
narrow (1-5 tissues)	0
moderate (6-20)	0
broad (>20)	1
unknown	0

Top tissues across cohort

Tissue	Cohort genes
diaphragm	1
right lung	1
visceral pleura	1

Per-gene tissue summary (top 30)

Symbol	Bgee breadth	FANTOM5 breadth	SCXA	Top tissues
TEK	223	broad	marker	right lung, diaphragm, visceral pleura

Protein interactions among cohort

Intra-cohort edges: 0.

Hub genes (top 10 by interactor count)

Symbol	Interactor count
TEK	2,762

Structural data

PDB: 1 · AlphaFold-only: 0 · No structure: 0

Cohort genes with PDB structures (top 30)

Symbol	UniProt	PDB entries
TEK	Q02763	17

Function

Pathway analysis

Distinct Reactome pathways touched by cohort: 7. Enrichment computed across 1 evidence-associated genes (1 with Reactome annotation).

Pathways by enrichment

Over-representation of cohort genes vs the genome-wide background (hypergeometric test, Benjamini-Hochberg FDR; fold = observed/expected over 1 annotated cohort genes). Counts and members are kept as ground-truth; sorted by enrichment.

Pathway	Cohort genes	Fold	FDR	Sample cohort genes
Tie2 Signaling	1	601.0×	0.012	TEK
MAPK1/MAPK3 signaling	1	131.3×	0.018	TEK
MAPK family signaling cascades	1	102.9×	0.018	TEK
Cell surface interactions at the vascular wall	1	95.2×	0.018	TEK
RAF/MAP kinase cascade	1	61.1×	0.023	TEK
Hemostasis	1	36.0×	0.032	TEK
Signal Transduction	1	10.2×	0.098	TEK

GO biological processes by enrichment

Over-representation of cohort genes vs the genome-wide background (hypergeometric test, Benjamini-Hochberg FDR; fold = observed/expected over 1 annotated cohort genes). Counts and members are kept as ground-truth; sorted by enrichment.

GO term	Cohort genes	Fold	FDR	Sample cohort genes
regulation of endothelial cell apoptotic process	1	8426.0×	0.002	TEK
glomerulus vasculature development	1	4213.0×	0.002	TEK
regulation of establishment or maintenance of cell polarity	1	3370.4×	0.002	TEK
Tie signaling pathway	1	3370.4×	0.002	TEK
regulation of vascular permeability	1	1123.5×	0.004	TEK
heart trabecula formation	1	1123.5×	0.004	TEK
definitive hemopoiesis	1	936.2×	0.004	TEK
positive regulation of Rac protein signal transduction	1	648.1×	0.004	TEK
positive regulation of focal adhesion assembly	1	648.1×	0.004	TEK
positive regulation of intracellular signal transduction	1	648.1×	0.004	TEK
positive regulation of Rho protein signal transduction	1	581.1×	0.004	TEK
endothelial cell proliferation	1	543.6×	0.004	TEK
negative regulation of endothelial cell apoptotic process	1	495.6×	0.004	TEK
sprouting angiogenesis	1	481.5×	0.004	TEK
substrate adhesion-dependent cell spreading	1	343.9×	0.006	TEK
positive regulation of endothelial cell migration	1	251.5×	0.007	TEK
positive regulation of endothelial cell proliferation	1	230.8×	0.008	TEK
cellular response to mechanical stimulus	1	216.1×	0.008	TEK
cell surface receptor protein tyrosine kinase signaling pathway	1	173.7×	0.009	TEK
negative regulation of angiogenesis	1	168.5×	0.009	TEK
negative regulation of inflammatory response	1	137.0×	0.010	TEK
positive regulation of angiogenesis	1	115.4×	0.012	TEK
positive regulation of ERK1 and ERK2 cascade	1	85.1×	0.015	TEK
positive regulation of MAPK cascade	1	80.6×	0.015	TEK
heart development	1	78.8×	0.015	TEK
positive regulation of phosphatidylinositol 3-kinase/protein kinase B signal transduction	1	78.4×	0.015	TEK
cell-cell signaling	1	69.6×	0.016	TEK
cell surface receptor signaling pathway	1	64.1×	0.017	TEK
angiogenesis	1	62.4×	0.017	TEK
negative regulation of apoptotic process	1	34.8×	0.029	TEK

Therapeutics

Drug target analysis

Approved (phase 4): 1 · Phase ≥3: 1 · Phased (≥1): 1 · Undrugged: 0

Druggability breadth: 1 of 1 evidence-associated genes (100%) have a ChEMBL target (buckets above are over the deeply-mined display cohort).

Genes with an approved drug

The molecule shown is one approved compound that hits the gene — not necessarily a drug of choice or one indicated for this disease.

Symbol	Example approved molecule
TEK	CETIRIZINE

Top cohort targets by molecule count

Symbol	Molecules	Max phase
TEK	46	4

Drugs targeting cohort genes (top 30)

Molecule	Max phase	Targets in cohort
CETIRIZINE	4	TEK
FEDRATINIB	4	TEK
TIVOZANIB	4	TEK
AXITINIB	4	TEK
SORAFENIB	4	TEK
NICLOSAMIDE	4	TEK
AMPICILLIN	4	TEK
NERATINIB	4	TEK
INFIGRATINIB PHOSPHATE	4	TEK
INFIGRATINIB	4	TEK
REGORAFENIB	4	TEK
CABOZANTINIB	4	TEK
VANDETANIB	4	TEK
NILOTINIB	4	TEK
BOSUTINIB	4	TEK
PAZOPANIB	4	TEK
NINTEDANIB	4	TEK
QUIZARTINIB	4	TEK
CRIZOTINIB	4	TEK
MIDOSTAURIN	4	TEK
LOPERAMIDE	4	TEK
LINIFANIB	3	TEK
BRIVANIB	3	TEK
CEDIRANIB	3	TEK
LESTAURTINIB	3	TEK
DORAMAPIMOD	2	TEK
FORETINIB	2	TEK
REBASTINIB	2	TEK
CEP-11981	2	TEK
DEFOSBARASERTIB	2	TEK

Bioactivity and enzyme data

Enzyme cohort genes (≥1 EC): 1.

Cohort genes with ChEMBL bioactivity (full, sorted by assay count)

Symbol	Assays	Type breakdown
TEK	707	Binding:701, Functional:4, ADMET:2

Cohort enzymes (BRENDA EC)

Symbol	EC numbers	Names
TEK	2.7.10.1	receptor protein-tyrosine kinase

Cohort genes with high screening signal

≥100 ChEMBL assays — a studied-ness signal; see Therapeutics for approved-drug status.

Symbol	ChEMBL assays
TEK	707

Pharmacogenomics

Cohort genes with a PharmGKB record: 1; with CPIC/DPWG dosing guidelines: 0.

No cohort gene has a CPIC/DPWG genotype-guided dosing guideline (PharmGKB).

Chemical tractability of cohort targets

30 approved/phased compounds have measured bioactivity against a cohort gene (and aren’t yet in disease-level trials). This is a research / tractability signal, NOT a therapeutic recommendation — a bioactivity row often reflects off-target or screening binding (e.g. promiscuous kinase inhibitors against a cohort kinase), implying no disease mechanism.

Compound	Max phase	Cohort target (bioactivity)
CETIRIZINE	4	TEK
FEDRATINIB	4	TEK
TIVOZANIB	4	TEK
AXITINIB	4	TEK
SORAFENIB	4	TEK
NICLOSAMIDE	4	TEK
AMPICILLIN	4	TEK
NERATINIB	4	TEK
INFIGRATINIB PHOSPHATE	4	TEK
INFIGRATINIB	4	TEK
REGORAFENIB	4	TEK
CABOZANTINIB	4	TEK
VANDETANIB	4	TEK
NILOTINIB	4	TEK
BOSUTINIB	4	TEK
PAZOPANIB	4	TEK
NINTEDANIB	4	TEK
QUIZARTINIB	4	TEK
CRIZOTINIB	4	TEK
MIDOSTAURIN	4	TEK
LOPERAMIDE	4	TEK
LINIFANIB	3	TEK
BRIVANIB	3	TEK
CEDIRANIB	3	TEK
LESTAURTINIB	3	TEK
DORAMAPIMOD	2	TEK
FORETINIB	2	TEK
REBASTINIB	2	TEK
CEP-11981	2	TEK
DEFOSBARASERTIB	2	TEK

Druggability pyramid

Cohort genes binned by druggability tier (high → low):

Tier	Definition	Genes	Symbols
A	Approved (phase 4 drug)	1	TEK
B	Phased (≥1) drug, not yet approved	0
C	Druggable family + PDB, no drug	0
D	Druggable family + AlphaFold only, no drug	0
E	Difficult family or no structure, no drug	0

Undrugged target profiles

0 cohort genes are undrugged. Ranked by ‘starting-point quality’ (assay depth + drugged-partner adjacency).

Clinical trials & evidence

Clinical trials

Clinical trials: 0.