HSD11B2

Summary

HSD11B2 (hydroxysteroid 11-beta dehydrogenase 2, HGNC:5209) is a protein-coding gene on chromosome 16q22.1, encoding 11-beta-hydroxysteroid dehydrogenase type 2 (P80365). Catalyzes the conversion of biologically active 11beta-hydroxyglucocorticoids (11beta-hydroxysteroid) such as cortisol, to inactive 11-ketoglucocorticoids (11-oxosteroid) such as cortisone, in the presence of NAD(+).

There are at least two isozymes of the corticosteroid 11-beta-dehydrogenase, a microsomal enzyme complex responsible for the interconversion of cortisol and cortisone. The type I isozyme has both 11-beta-dehydrogenase (cortisol to cortisone) and 11-oxoreductase (cortisone to cortisol) activities. The type II isozyme, encoded by this gene, has only 11-beta-dehydrogenase activity. In aldosterone-selective epithelial tissues such as the kidney, the type II isozyme catalyzes the glucocorticoid cortisol to the inactive metabolite cortisone, thus preventing illicit activation of the mineralocorticoid receptor. In tissues that do not express the mineralocorticoid receptor, such as the placenta and testis, it protects cells from the growth-inhibiting and/or pro-apoptotic effects of cortisol, particularly during embryonic development. Mutations in this gene cause the syndrome of apparent mineralocorticoid excess and hypertension.

Source: NCBI Gene 3291 — RefSeq curated summary.

At a glance

• Gene–disease (curated): apparent mineralocorticoid excess (Definitive, ClinGen)
• GWAS associations: 3
• Clinical variants (ClinVar): 211 total — 11 pathogenic, 8 likely-pathogenic
• Phenotypes (HPO): 22
• Druggable target: yes — 5 molecules with ChEMBL bioactivity
• MANE Select transcript: NM_000196

Identifiers

Gene identifiers

Field	Value
HGNC ID	HGNC:5209
Approved symbol	HSD11B2
Name	hydroxysteroid 11-beta dehydrogenase 2
Location	16q22.1
Locus type	gene with protein product
Status	Approved
Aliases	SDR9C3
Ensembl gene	ENSG00000176387
Ensembl biotype	protein_coding
OMIM	614232
Entrez	3291

Gene structure

Transcript identifiers

Ensembl transcripts: 7 — 4 protein_coding, 1 nonsense_mediated_decay, 1 protein_coding_CDS_not_defined, 1 retained_intron

ENST00000326152, ENST00000566606, ENST00000567684, ENST00000569303, ENST00000855495, ENST00000855496, ENST00000855497

RefSeq mRNA: 1 — MANE Select: NM_000196 NM_000196

CCDS: CCDS10837

Canonical transcript exons

ENST00000326152 — 5 exons

Exon	Start	End
ENSE00001268475	67436249	67436386
ENSE00001268498	67436588	67437553
ENSE00001303320	67431121	67431513
ENSE00003484101	67435957	67436142
ENSE00003569783	67435628	67435840

Expression profiles

Bgee: expression breadth ubiquitous, 174 present calls, max score 99.28.

FANTOM5 (CAGE): breadth broad, TPM avg 2.9950 / max 345.9402, expressed in 549 samples.

FANTOM5 promoters (4 alternative TSS)

Promoter ID	TPM avg	Samples expressed
154626	2.1257	323
154624	0.5465	271
154628	0.2064	94
154627	0.1164	55

Top tissues by expression

289 total, by Bgee expression score (0-100, higher = more expressed):

Tissue	Anatomy ID	Expression score	Quality
mucosa of transverse colon	UBERON:0004991	99.28	gold quality
renal medulla	UBERON:0000362	98.61	gold quality
rectum	UBERON:0001052	98.57	gold quality
adult mammalian kidney	UBERON:0000082	98.38	gold quality
metanephros cortex	UBERON:0010533	98.32	gold quality
ileal mucosa	UBERON:0000331	96.53	gold quality
parotid gland	UBERON:0001831	96.21	gold quality
colonic mucosa	UBERON:0000317	95.62	gold quality
skin of leg	UBERON:0001511	95.25	gold quality
mucosa of sigmoid colon	UBERON:0004993	94.75	gold quality
kidney	UBERON:0002113	94.47	gold quality
saliva-secreting gland	UBERON:0001044	94.43	gold quality
skin of abdomen	UBERON:0001416	93.93	gold quality
minor salivary gland	UBERON:0001830	93.65	gold quality
small intestine Peyer’s patch	UBERON:0003454	93.13	gold quality
transverse colon	UBERON:0001157	93.06	gold quality
nephron tubule	UBERON:0001231	92.54	gold quality
cortex of kidney	UBERON:0001225	91.47	gold quality
kidney epithelium	UBERON:0004819	90.35	gold quality
zone of skin	UBERON:0000014	90.32	gold quality
small intestine	UBERON:0002108	90.24	gold quality
olfactory segment of nasal mucosa	UBERON:0005386	90.02	gold quality
mouth mucosa	UBERON:0003729	87.53	gold quality
placenta	UBERON:0001987	86.97	gold quality
colonic epithelium	UBERON:0000397	86.48	gold quality
renal glomerulus	UBERON:0000074	86.23	gold quality
intestine	UBERON:0000160	86.07	gold quality
metanephros	UBERON:0000081	85.68	gold quality
large intestine	UBERON:0000059	85.47	gold quality
metanephric glomerulus	UBERON:0004736	85.22	silver quality

Single-cell (SCXA)

Detected in 4 experiment(s), a significant marker in 3.

Experiment	Marker?	Max mean expression
E-GEOD-131882	yes	1300.12
E-CURD-119	yes	1206.69
E-GEOD-99795	no	154.62
E-ANND-3	no	0.00

Regulation

Is transcription factor: no

Upstream regulators (CollecTRI, top): CEBPB, EGR1, ESR1, MYC, NF1, NFIC, NFKB1, NFKB, NR3C1, PGR, PPARD, RELA, SP1, SP3, STAT5A

miRNA regulators (miRDB)

43 targeting HSD11B2, top 30 by miRDB confidence (max_score; target_count = how many genes the miRNA targets in total — lower means more specific):

miRNA	Max score	Avg score	miRNA target_count
HSA-MIR-101-3P	99.94	75.03	2230
HSA-MIR-4525	99.94	64.38	675
HSA-MIR-515-5P	99.92	69.82	2343
HSA-MIR-519E-5P	99.92	69.62	2358
HSA-MIR-4731-5P	99.89	67.23	2537
HSA-MIR-7110-5P	99.80	67.84	1712
HSA-MIR-6842-5P	99.80	67.54	1587
HSA-MIR-10394-5P	99.65	66.83	1852
HSA-MIR-1205	99.65	66.76	1826
HSA-MIR-6752-5P	99.59	67.32	1243
HSA-MIR-6751-5P	99.56	64.99	1145
HSA-MIR-4649-3P	99.56	66.90	1783
HSA-MIR-17-3P	99.55	66.77	1311
HSA-MIR-4437	99.52	65.29	1266
HSA-MIR-1275	99.47	67.90	2749
HSA-MIR-5695	99.41	67.48	1047
HSA-MIR-3678-3P	99.31	67.10	1432
HSA-MIR-4505	99.27	67.81	2678
HSA-MIR-5787	99.22	67.86	2628
HSA-MIR-6803-5P	99.19	63.90	1026
HSA-MIR-544B	99.18	67.41	1632
HSA-MIR-4687-5P	99.14	66.26	488
HSA-MIR-3688-5P	99.12	69.67	1091
HSA-MIR-511-5P	98.97	70.94	2268
HSA-MIR-2467-3P	98.65	67.18	1969
HSA-MIR-1227-5P	98.65	65.32	1549
HSA-MIR-8060	98.61	66.93	1187
HSA-MIR-5089-5P	98.45	66.06	1388
HSA-MIR-4665-5P	97.91	67.69	1536
HSA-MIR-637	97.91	64.05	1517

Literature-anchored findings (GeneRIF, showing 40)

• Effect of cellular differentiation on 11beta-hydroxysteroid dehydrogenase activity in the intestine (PMID:11755176)
• effect of ATP on activity in human placental microsomes (PMID:11787058)
• in vivo footprinting of promoter and cell-specific regulation by Sp1 and Sp3 (PMID:11850421)
• Weak associations between the HSD11B2 gene, type 1 diabetes mellitus and nephropathy. (PMID:11916625)
• Human adrenal cortex and aldosterone secreting adenomas express both 11beta-hydroxysteroid dehydrogenase type 1 and type 2 genes. (PMID:11956655)
• chenodeoxycholic acid and deoxycholic acid, by inhibiting 11 beta HSD2, mediate cortisol-dependent nuclear translocation and transcriptional activation of Mineralocorticoid receptor (PMID:12015312)
• 11beta-Hydroxysteroid dehydrogenase types 1 and 2 are up- and downregulated in cortisol-secreting adrenal adenomas. (PMID:12109593)
• The expression of 11 beta-hydroxysteroid dehydrogenase type 2 is induced during trophoblast differentiation: effects of hypoxia. (PMID:12161498)
• first report to suggest that 11 beta-hydroxysteroid dehydrogenase 2 is O(2) dependent in first and third trimester placenta during human gestation (PMID:12364476)
• In small preterm infants, reduced placental 11 beta-HSD2 function is asociated with low relative birth weight and severe fetal distress. (PMID:12519895)
• Nonfunctioning adenomas and those causing preclinical and overt Cushing’s syndrome may represent a continuum with clinical manifestations depending mainly on tumor size and HSD11B2 expression levels. (PMID:12574226)
• determination of abnormal expression in pituitary adenomas (PMID:12642869)
• 11 beta-Hydroxysteroid dehydrogenase type 2 (11 beta-HSD2) plays a crucial role in converting hormonally active cortisol to inactive cortisone, thereby conferring specificity on the mineralocorticoid receptor. Review. (PMID:12788832)
• Homozygous mutation in exon 4 Asp223Asn changed the enzyme’s surface electrostatic potential affecting the cofactor and substrate enzyme-binding capacity. (PMID:12788846)
• Late-onset apparent mineralocorticoid excess caused by novel compound heterozygous mutations in the HSD11B2 gene. (PMID:12860834)
• Ang II decreases activity of 11beta-HSD2 by AT2 receptor- and MAPK-dependent mechanism. Decreased activity of 11beta-HSD2 increases intracellular availability of cortisol. May be relevant for pathogenesis of hypertension and preeclampsia. (PMID:12911547)
• An increase in the expression of 11 beta-HSD2 may result in faster glucocorticoid breakdown in lung cells in patients with acute respiratory distress syndrome (ARDS). (PMID:14629298)
• results suggest that renal 11-hydroxysteroid dehydrogenase 2 is a main factor controlling the equilibrium of plasma cortisol and cortisone concentrations in the periphery (PMID:14681848)
• Patients with essential hypertension and without any biological evidence of aldosterone excess have an overall significant 39% reduction in ex vivo HSD2 catalytic activity in sweat gland ducts, as compared with normotensive subjects. (PMID:14981055)
• Decrease of 11betaHSD2 mRNA abundance and enzyme activity is associated with colorectal cancer (PMID:15172126)
• The antiproliferative effects of glucocorticosteroids were reversed and total cell growth boosted by overexpression of 11beta-HSD2. The increase in cell proliferation was attained by low 11beta-HSD2 overexpression. (PMID:15305225)
• These results indicate a role for DNA methylation in 11 beta-hydroxysteroid dehydrogenase type 2 gene repression and suggest an epigenetic mechanism affecting this gene causally linked with hypertension. (PMID:15489962)
• 11beta-HSD2 is an additional target for PPAR delta, which may regulate human placental function (PMID:15591138)
• Critical role of 11betaHSD2 for ensuring selectivity of the mineralocarticoid receptors in the distal nephron (PMID:15643119)
• hypertensives with suppressed renin activity may have an impairment in the cortisol inactivation catalyzed by the enzyme 11betaHSD2, which could be associated with the length of CA-repeat microsatellite in intron 1 of the HSD11B2 gene (PMID:15643127)
• Reduced renal 11beta-HSD2 expression may lead to occupancy of the MR by glucocorticoids such as cortisol and may contribute to the increased sodium retention seen in patients with impaired renal function (PMID:16061836)
• Study identifies placental 11 beta-HSD2 as a novel molecular target of cadmium. (PMID:16144812)
• The reduced placental 11beta-HSD2 in fetal growth restriction is not due to intrinsic abnormalities in trophoblast cells, but likely a result of extrinsic factors associated with FGR. (PMID:16271275)
• lung inflammation reduces local glucocorticoid breakdown and augments glucocorticoid action in the lung by down-regulating 11beta-HSD2 via multiple mechanisms (PMID:16272800)
• 11BetaHSD-2 and GR were expressed across the mensrual cycle. (PMID:16406280)
• missense mutations in HSD11B2 do not substantially contribute to essential hypertension in Japanese (PMID:16778331)
• The 3 most significantly overexpressed genes were in rheumatoid arthritis were laeverin, 11beta-hydroxysteroid dehydrogenase type 2 (a steroid pathway enzyme), and cysteine-rich, angiogenic inducer 61 (a known angiogenic factor). (PMID:16804865)
• Data show that protein kinase A pathway activators such as arginine vasopressin induce, and protein kinase C pathway activators repress the expression of 11beta-hydroxysteroid dehydrogenase type 2 in human renal epithelial cells. (PMID:16872738)
• renal 11beta-hydroxysteroid dehydrogenase type 2 is an important regulatory factor of renal Na and K (PMID:16979406)
• Data show that type 2 1beta-hydroxysteroid dehydrogenase activity in ovarian cancer specimens is significantly higher than enzyme activity measured in normal post-menopausal ovarian tissue. (PMID:17028049)
• Data show that 11-beta hydroxysteroid dehydrogenase type 2 (HSD2) protein and activity levels increase with differentiation of alveolar type II cells, and that HSD2 protein levels are regulated by 17-beta estradiol in male fetal lung tissue. (PMID:17515840)
• skeletal muscle 11beta-HSD1 and 11beta-HSD2 are altered in diabetes, which together may reduce intracellular cortisol generation, potentially conferring metabolic protection (PMID:17519316)
• conclude that the mechanism of glucocorticoid-induced HSD11B2 expression is mainly mediated by cooperation between glucocorticoid receptor and nuclear factor 1 on the HSD11B2 promoter (PMID:17551100)
• The effect of LOX metabolites on HSD11B2 is mediated by their stimulation of endogenous progesterone output. (PMID:18032417)
• A role for an attenuated placental as well as fetal 11beta-HSD2 in the pathogenesis of intrauterine growth restriction. (PMID:18061258)

Cross-species orthologs

3 orthologs

Organism	Symbol	Gene ID
danio_rerio	hsd11b2	ENSDARG00000001975
mus_musculus	Hsd11b2	ENSMUSG00000031891
rattus_norvegicus	Hsd11b2	ENSRNOG00000017084

Paralogs (25): HSD17B6 (ENSG00000025423), RDH11 (ENSG00000072042), HSD17B10 (ENSG00000072506), DHRS9 (ENSG00000073737), HSD17B2 (ENSG00000086696), HSD17B14 (ENSG00000087076), DHRS12 (ENSG00000102796), HSDL1 (ENSG00000103160), HSD17B1 (ENSG00000108786), RDH10 (ENSG00000121039), HSD17B3 (ENSG00000130948), HSD17B7 (ENSG00000132196), HSD17B4 (ENSG00000133835), RDH5 (ENSG00000135437), RDH16 (ENSG00000139547), RDH12 (ENSG00000139988), HSD17B12 (ENSG00000149084), BDH1 (ENSG00000161267), DHRS3 (ENSG00000162496), SDR9C7 (ENSG00000170426), HSD17B13 (ENSG00000170509), SDR16C5 (ENSG00000170786), WWOX (ENSG00000186153), HSD17B11 (ENSG00000198189), HSD17B8 (ENSG00000204228)

Protein

Protein identifiers

11-beta-hydroxysteroid dehydrogenase type 2 — P80365 (reviewed: P80365)

Alternative names: 11-beta-hydroxysteroid dehydrogenase type II, Corticosteroid 11-beta-dehydrogenase isozyme 2, NAD-dependent 11-beta-hydroxysteroid dehydrogenase, Short chain dehydrogenase/reductase family 9C member 3

All UniProt accessions (2): P80365, R4GN04

UniProt curated annotations — full annotation on UniProt →

Function. Catalyzes the conversion of biologically active 11beta-hydroxyglucocorticoids (11beta-hydroxysteroid) such as cortisol, to inactive 11-ketoglucocorticoids (11-oxosteroid) such as cortisone, in the presence of NAD(+). Functions as a dehydrogenase (oxidase), thereby decreasing the concentration of active glucocorticoids, thus protecting the nonselective mineralocorticoid receptor from occupation by glucocorticoids. Plays an important role in maintaining glucocorticoids balance during preimplantation and protects the fetus from excessive maternal corticosterone exposure. Catalyzes the oxidation of 11beta-hydroxytestosterone (11beta,17beta-dihydroxyandrost-4-ene-3-one) to 11-ketotestosterone (17beta-hydroxyandrost-4-ene-3,11-dione), a major bioactive androgen. Catalyzes the conversion of 11beta-hydroxyandrostenedione (11beta-hydroxyandrost-4-ene-3,17-dione) to 11-ketoandrostenedione (androst-4-ene-3,11,17-trione), which can be further metabolized to 11-ketotestosterone. Converts 7-beta-25-dihydroxycholesterol to 7-oxo-25-hydroxycholesterol in vitro. 7-beta-25-dihydroxycholesterol (not 7-oxo-25-hydroxycholesterol) acts as a ligand for the G-protein-coupled receptor (GPCR) Epstein-Barr virus-induced gene 2 (EBI2) and may thereby regulate immune cell migration. May protect ovulating oocytes and fertilizing spermatozoa from the adverse effects of cortisol.

Subunit / interactions. Interacts with ligand-free cytoplasmic NR3C2.

Subcellular location. Microsome. Endoplasmic reticulum.

Tissue specificity. Expressed in kidney, placenta, pancreas, prostate, ovary, small intestine and colon, and in lower levels in the spleen and testis. At midgestation, expressed at high levels in placenta and in fetal kidney and, at much lower levels, in fetal lung and testis.

Disease relevance. Apparent mineralocorticoid excess (AME) [MIM:218030] An autosomal recessive form of low-renin hypertension. It is usually diagnosed within the first years of life and is characterized by polyuria and polydipsia, failure to thrive, hypernatremia, severe hypertension with low renin and aldosterone levels, profound hypokalemia with metabolic alkalosis, and most often nephrocalcinosis. The disease is caused by variants affecting the gene represented in this entry.

Activity regulation. Inhibited by glycyrrhetinic acid (derived from liquorice).

Pathway. Steroid metabolism.

Miscellaneous. Consumption of large amounts of liquorice can lead to apparent mineralocorticoid excess and hypertension.

Similarity. Belongs to the short-chain dehydrogenases/reductases (SDR) family.

RefSeq proteins (1): NP_000187* (*=MANE)

Domains & families (InterPro)

ID	Name	Type
IPR002347	SDR_fam	Family
IPR020904	Sc_DH/Rdtase_CS	Conserved_site
IPR036291	NAD(P)-bd_dom_sf	Homologous_superfamily

Pfam: PF00106

Enzyme classification (BRENDA):

• EC 1.1.1.146 — 11beta-hydroxysteroid dehydrogenase (BRENDA: 26 organisms, 286 substrates, 1331 inhibitors, 120 Km, 10 kcat entries)
• EC 1.1.1.B40 — (BRENDA: organisms, substrates, inhibitors, Km, kcat entries)

Substrate kinetics (BRENDA)

33 substrates with measured Km, best-characterized 15. Km ranges are aggregated across organisms/conditions.

Substrate	Km (mM)	Measurements
CORTISONE	0.0003–0.193	16
CORTISOL	0.0002–0.1	14
11BETA,17,21-TRIHYDROXY-PREGN-4-ENE-3,20-DIONE	0.0014–0.027	9
11BETA,21-DIHYDROXYPREGN-4-EN-3,20-DIONE	—	9
CORTICOSTERONE	0.0003–0.043	8
11-DEHYDROCORTICOSTERONE	0.0002–0.0073	7
17,21-DIHYDROXY-PREGN-4-ENE-3,11,20-TRIONE	0.0038–0.0095	6
NADP+	—	6
7BETA-HYDROXYCHOLESTEROL	0.0007–3.5	5
21-HYDROXY-PREGN-4-EN-3,11,20-TRIONE	0.0014–0.0028	4
7-OXOCHOLESTEROL	0.0004–0.0005	3
NADPH	0.0036–0.0037	3
11BETA-HYDROXYPROGESTERONE	—	2
11BETA-HYDROXYTESTOSTERONE	0.0001	2
5,5-DIMETHYL-3-(3-FLUORPHENYL)-4-(4-METHYLSULPHO	0.581–0.961	2

Catalyzed reactions (Rhea), 5 shown:

• corticosterone + NAD(+) = 11-dehydrocorticosterone + NADH + H(+) (RHEA:42204)
• cortisol + NAD(+) = cortisone + NADH + H(+) (RHEA:50208)
• an 11beta-hydroxysteroid + NAD(+) = an 11-oxosteroid + NADH + H(+) (RHEA:53116)
• 11beta,17beta-dihydroxyandrost-4-ene-3-one + NAD(+) = 17beta-hydroxyandrost-4-ene-3,11-dione + NADH + H(+) (RHEA:69368)
• 11beta-hydroxyandrost-4-ene-3,17-dione + NAD(+) = androst-4-ene-3,11,17-trione + NADH + H(+) (RHEA:69408)

UniProt features (41 total): sequence variant 20, mutagenesis site 9, sequence conflict 4, region of interest 2, compositionally biased region 2, binding site 2, chain 1, active site 1

Structure

Experimental structures (PDB)

0 structures.

Predicted structure (AlphaFold)

Model	pLDDT	Fraction very-high
AF-P80365-F1	87.49	0.60

Functional residue map

Curated UniProt residues grouped by drug-discovery relevance — catalytic, ligand-binding, modification, and mutation-validated positions. Source: UniProtKB sequence features.

Catalytic / active sites (1): 232 (proton acceptor)

Ligand- & substrate-binding residues (2): 82–111; 219

Mutagenesis-validated functional residues (9):

Position	Phenotype
115	abolishes cofactor specificity.
335	reduced enzyme activity.
335	no effect on enzyme activity.
336	almost complete loss of enzyme activity.
336	reduced enzyme activity.
337	almost complete loss of enzyme activity.
337	reduced enzyme activity.
338	complete loss of enzyme activity.
339	reduced enzyme activity.

Function

Pathways and Gene Ontology

Reactome pathways

2 pathways

ID	Pathway
R-HSA-194002	Glucocorticoid biosynthesis
R-HSA-9757110	Prednisone ADME

MSigDB gene sets: 231 (showing top): GOBP_RESPONSE_TO_NITROGEN_COMPOUND, MYOGENIN_Q6, GOBP_REGULATION_OF_BLOOD_PRESSURE, chr16q22, GOBP_CIRCULATORY_SYSTEM_PROCESS, PEREZ_TP63_TARGETS, GOBP_RESPONSE_TO_CORTICOSTEROID, GOBP_GLUCOCORTICOID_METABOLIC_PROCESS, GCANCTGNY_MYOD_Q6, GOBP_RENAL_SYSTEM_PROCESS_INVOLVED_IN_REGULATION_OF_BLOOD_VOLUME, GRAESSMANN_APOPTOSIS_BY_SERUM_DEPRIVATION_UP, GRAESSMANN_RESPONSE_TO_MC_AND_SERUM_DEPRIVATION_UP, GRAESSMANN_APOPTOSIS_BY_DOXORUBICIN_UP, GRAESSMANN_RESPONSE_TO_MC_AND_DOXORUBICIN_UP, GOBP_REGULATION_OF_SYSTEMIC_ARTERIAL_BLOOD_PRESSURE

GO Biological Process (12): response to hypoxia (GO:0001666), regulation of blood volume by renal aldosterone (GO:0002017), female pregnancy (GO:0007565), glucocorticoid metabolic process (GO:0008211), response to xenobiotic stimulus (GO:0009410), response to food (GO:0032094), response to insulin (GO:0032868), cortisol metabolic process (GO:0034650), response to glucocorticoid (GO:0051384), lipid metabolic process (GO:0006629), steroid metabolic process (GO:0008202), response to steroid hormone (GO:0048545)

GO Molecular Function (5): steroid binding (GO:0005496), NAD binding (GO:0051287), 11-beta-hydroxysteroid dehydrogenase (NAD+) activity (GO:0070523), oxidoreductase activity (GO:0016491), oxidoreductase activity, acting on the CH-OH group of donors, NAD or NADP as acceptor (GO:0016616)

GO Cellular Component (3): endoplasmic reticulum membrane (GO:0005789), endoplasmic reticulum (GO:0005783), membrane (GO:0016020)

Reactome top-level categories

Rollup of top-2 pathways:

Category	Pathways
Metabolism of steroid hormones	1
Drug ADME	1

GO top-level categories

Rollup of top GO terms by namespace:

Category	Terms
response to chemical	2
response to stress	1
response to decreased oxygen levels	1
regulation of systemic arterial blood pressure by hormone	1
positive regulation of systemic arterial blood pressure	1
multi-organism reproductive process	1
multi-multicellular organism process	1
steroid metabolic process	1
response to nutrient levels	1
response to peptide hormone	1
glucocorticoid metabolic process	1
primary alcohol metabolic process	1
ketone metabolic process	1
olefinic compound metabolic process	1
tertiary alcohol metabolic process	1
response to corticosteroid	1
primary metabolic process	1
lipid metabolic process	1
response to hormone	1
response to lipid	1
lipid binding	1
adenyl nucleotide binding	1
steroid dehydrogenase activity, acting on the CH-OH group of donors, NAD or NADP as acceptor	1
catalytic activity	1
oxidoreductase activity, acting on CH-OH group of donors	1
organelle membrane	1
nuclear outer membrane-endoplasmic reticulum membrane network	1
endoplasmic reticulum subcompartment	1
cytoplasm	1
endomembrane system	1
intracellular membrane-bounded organelle	1
cellular anatomical structure	1

Protein interactions and networks

STRING

1288 interactions, top by confidence (×1000):

Protein A	Protein B	Partner UniProt	Score
HSD11B2	CYP11B1	P15538	919
HSD11B2	NR3C2	P08235	918
HSD11B2	CYP11B2	P19099	901
HSD11B2	H6PD	O95479	878
HSD11B2	POMC	P01189	868
HSD11B2	CYP17A1	P05093	856
HSD11B2	CYP11A1	P05108	851
HSD11B2	CYP21A2	P04033	846
HSD11B2	NR3C1	P04150	816
HSD11B2	HPGD	P15428	804
HSD11B2	SRD5A1	P18405	800
HSD11B2	CRH	P06850	784
HSD11B2	MC2R	Q01718	770
HSD11B2	REN	P00797	757
HSD11B2	AKR1D1	P51857	752

IntAct

0 interactions, top by confidence:

BioGRID (12): HSD11B2 (Affinity Capture-MS), HSD11B2 (Affinity Capture-RNA), HSD11B2 (Affinity Capture-RNA), HSD11B2 (Affinity Capture-MS), HSD11B2 (Proximity Label-MS), HSD11B2 (Affinity Capture-Western), HSD11B2 (Affinity Capture-Western), HSD11B2 (Biochemical Activity), HSD11B2 (Biochemical Activity), CTBP1 (Affinity Capture-Western), HSD11B2 (Affinity Capture-Western), HSD11B2 (Affinity Capture-Western)

ESM2 similar proteins: A0A0U1RPR8, A1A4J8, A6H751, A6H784, A7YY46, D3ZBP4, F1MH07, O08644, O15197, O19179, O43542, O43819, O43824, O75880, O88561, O88941, P0C0K6, P0C0K7, P0C7A1, P50233, P51839, P51840, P51976, P52785, P55203, P80365, Q02846, Q05932, Q08DH8, Q13724, Q3U6U5, Q5JTZ9, Q5K4L6, Q5SS80, Q5SUC9, Q69ZP3, Q80UM7, Q8N490, Q8NFI3, Q8TDZ2

Diamond homologs: A0A0E3D8L9, A0A140JWS5, A0A1L5BUG8, A0A2G0QDN4, A0A3R5XUE6, A0A8I6GJ95, A4IFM3, A6SG70, A7F8T1, A7IQF2, D2WKD9, D4YYG1, F1QLP1, O14756, O16881, O31680, O54909, O55240, O74628, O75452, O88451, P0A0H9, P0A0I0, P0A2C9, P0A2D0, P0AEK2, P0AEK3, P0AFP4, P0AFP5, P0CU71, P0DKC7, P14697, P16543, P16544, P23238, P25145, P28643, P29147, P37059, P37959

SIGNOR signaling

3 interactions.

A	Effect	B	Mechanism
EGR1	“down-regulates quantity by repression”	HSD11B2	“transcriptional regulation”
NfKb-p65/p50	“up-regulates quantity by expression”	HSD11B2	“transcriptional regulation”
PPARD	“down-regulates quantity by repression”	HSD11B2	“transcriptional regulation”

Disease & clinical

Clinical variants and AI predictions

ClinVar

211 variants total. Per-class counts are floors (≥ shown; pagination cap):

Classification	Count (floor)
Pathogenic	11
Likely pathogenic	8
Uncertain significance	115
Likely benign	50
Benign	9

Top pathogenic / likely-pathogenic (19)

Variant ID	HGVS	Classification
12093	NM_000196.4(HSD11B2):c.622C>T (p.Arg208Cys)	Pathogenic
12094	NM_000196.4(HSD11B2):c.637C>T (p.Arg213Cys)	Pathogenic
12095	NM_000196.4(HSD11B2):c.1009C>T (p.Arg337Cys)	Pathogenic
12098	NM_000196.4(HSD11B2):c.835C>T (p.Arg279Cys)	Pathogenic
12099	NM_000196.4(HSD11B2):c.680C>T (p.Pro227Leu)	Pathogenic
2033856	NM_000196.4(HSD11B2):c.83_177del (p.Leu28fs)	Pathogenic
2789381	NM_000196.4(HSD11B2):c.735dup (p.Phe246fs)	Pathogenic
2876313	NM_000196.4(HSD11B2):c.168_195del (p.Ala57fs)	Pathogenic
31131	NM_000196.4(HSD11B2):c.1012T>C (p.Tyr338His)	Pathogenic
31132	NM_000196.4(HSD11B2):c.77_78del (p.Arg25_Ser26insTer)	Pathogenic
974390	NM_000196.4(HSD11B2):c.1020del (p.Gly341fs)	Pathogenic
2137838	NM_000196.4(HSD11B2):c.556C>T (p.Arg186Cys)	Likely pathogenic
3581148	NM_000196.4(HSD11B2):c.433dup (p.Ile145fs)	Likely pathogenic
3581156	NM_000196.4(HSD11B2):c.662C>T (p.Ala221Val)	Likely pathogenic
3581157	NM_000196.4(HSD11B2):c.665-1G>A	Likely pathogenic
3581159	NM_000196.4(HSD11B2):c.665-1G>C	Likely pathogenic
3581160	NM_000196.4(HSD11B2):c.695_703del (p.Tyr232_Thr234del)	Likely pathogenic
3581165	NM_000196.4(HSD11B2):c.917_927del (p.Gln306fs)	Likely pathogenic
974391	NM_000196.4(HSD11B2):c.983C>T (p.Ala328Val)	Likely pathogenic

SpliceAI

804 predictions. Top by Δscore:

Variant	Effect	Δscore
16:67431510:ACCGG:A	donor_loss	1.0000
16:67431512:CGG:C	donor_loss	1.0000
16:67431514:G:GG	donor_gain	1.0000
16:67431514:G:T	donor_loss	1.0000
16:67431515:T:G	donor_loss	1.0000
16:67435841:G:GG	donor_gain	1.0000
16:67435941:T:TA	acceptor_gain	1.0000
16:67435946:T:TA	acceptor_gain	1.0000
16:67435948:T:TA	acceptor_gain	1.0000
16:67435952:CCCA:C	acceptor_loss	1.0000
16:67435954:CA:C	acceptor_loss	1.0000
16:67435955:A:AG	acceptor_gain	1.0000
16:67435955:A:G	acceptor_loss	1.0000
16:67435955:AG:A	acceptor_gain	1.0000
16:67435956:G:A	acceptor_loss	1.0000
16:67435956:G:GC	acceptor_gain	1.0000
16:67435956:GG:G	acceptor_gain	1.0000
16:67435956:GGC:G	acceptor_gain	1.0000
16:67435956:GGCC:G	acceptor_gain	1.0000
16:67435956:GGCCT:G	acceptor_gain	1.0000
16:67436139:GCGG:G	donor_gain	1.0000
16:67436140:CGGG:C	donor_loss	1.0000
16:67436141:GG:G	donor_gain	1.0000
16:67436142:GG:G	donor_gain	1.0000
16:67436143:G:GA	donor_loss	1.0000
16:67436144:T:A	donor_loss	1.0000
16:67436243:CCGCA:C	acceptor_loss	1.0000
16:67436244:CGCAG:C	acceptor_loss	1.0000
16:67436245:GCAG:G	acceptor_loss	1.0000
16:67436246:CA:C	acceptor_loss	1.0000

AlphaMissense

2559 scored. Top likely-pathogenic:

Variant	Protein change	am_pathogenicity
16:67436133:A:C	S219R	0.995
16:67436135:C:A	S219R	0.995
16:67436135:C:G	S219R	0.995
16:67436288:C:T	S235F	0.995
16:67436291:A:T	K236I	0.995
16:67435972:T:A	V165D	0.994
16:67436288:C:A	S235Y	0.994
16:67435658:C:A	A99D	0.993
16:67435976:C:A	N166K	0.992
16:67435976:C:G	N166K	0.992
16:67436297:C:A	A238D	0.992
16:67431508:T:A	I87N	0.991
16:67436116:G:C	R213P	0.991
16:67436122:T:A	V215E	0.991
16:67436363:T:A	I260N	0.991
16:67436377:T:C	F265L	0.991
16:67436379:C:A	F265L	0.991
16:67436379:C:G	F265L	0.991
16:67435969:T:C	L164P	0.990
16:67435632:T:G	C90W	0.989
16:67435682:T:C	F107S	0.989
16:67436356:A:C	S258R	0.989
16:67436358:C:A	S258R	0.989
16:67436358:C:G	S258R	0.989
16:67435667:T:C	L102P	0.988
16:67436292:A:C	K236N	0.988
16:67436292:A:T	K236N	0.988
16:67436333:T:C	L250P	0.988
16:67435631:G:A	C90Y	0.987
16:67435642:T:C	F94L	0.987

dbSNP variants (sampled 300 via entrez): RS1000032379 (16:67435961 G>A), RS1000061644 (16:67429773 T>C), RS1000085328 (16:67432384 G>A), RS1000541781 (16:67435084 G>T), RS1000606523 (16:67436349 C>T), RS1000636396 (16:67437110 T>C), RS1001242751 (16:67429302 T>TG), RS1002098242 (16:67432290 T>G), RS1002637010 (16:67434537 A>G), RS1003017986 (16:67435015 TGA>T), RS1003049396 (16:67434455 G>A), RS1003386383 (16:67432679 C>A), RS1003967640 (16:67432050 T>G), RS1006132034 (16:67427828 T>C,G), RS1006189913 (16:67433285 G>A,C)

Disease associations

OMIM: gene MIM:614232 | disease phenotypes: MIM:218030

GenCC curated gene-disease

Disease	Classification	Inheritance
apparent mineralocorticoid excess	Strong	Autosomal recessive

ClinGen Gene-Disease Validity (1)

Expert-panel classifications — Definitive > Strong > Moderate > Limited > Disputed > Refuted.

Disease	Classification	Inheritance
apparent mineralocorticoid excess	Definitive	AR

Mondo (1): apparent mineralocorticoid excess (MONDO:0009025)

Orphanet (1): Apparent mineralocorticoid excess (Orphanet:320)

HPO phenotypes

22 total (22 of 22 shown, HPO-id order):

HPO	Term
HP:0000007	Autosomal recessive inheritance
HP:0000083	Renal insufficiency
HP:0000121	Nephrocalcinosis
HP:0000822	Hypertension
HP:0001095	Hypertensive retinopathy
HP:0001297	Stroke
HP:0001508	Failure to thrive
HP:0001510	Growth delay
HP:0001511	Intrauterine growth retardation
HP:0001518	Small for gestational age
HP:0001712	Left ventricular hypertrophy
HP:0001959	Polydipsia
HP:0001960	Hypokalemic metabolic alkalosis
HP:0002900	Hypokalemia
HP:0003351	Decreased circulating renin concentration
HP:0004319	Decreased circulating aldosterone concentration
HP:0004322	Short stature
HP:0011463	Childhood onset
HP:0011731	Abnormality of circulating cortisol level
HP:0012603	Abnormal urine sodium concentration
HP:0012606	Renal sodium wasting
HP:0200114	Metabolic alkalosis

GWAS associations

3 associations (top):

Study	Trait	p-value
GCST004518_2	Waist-to-hip ratio adjusted for body mass index	5.000000e-08
GCST005751_5	Empathy quotient	8.000000e-07
GCST010002_113	Refractive error	2.000000e-14

EFO canonical traits (2, from GWAS)

EFO ID	Trait name
EFO:0007788	BMI-adjusted waist-hip ratio
EFO:0009183	empathy measurement

MeSH disease descriptors (1)

Descriptor	Name	Tree numbers
D043204	Mineralocorticoid Excess Syndrome, Apparent	C16.320.565.925.500; C18.452.648.925.500

Drugs & pharmacology

Drug and pharmacology data

Is drug target: yes

ChEMBL targets (2): CHEMBL3542430 (PROTEIN FAMILY), CHEMBL3746 (SINGLE PROTEIN)

Molecules with ChEMBL bioactivity

5 molecules (phase ≥1), by development phase (incl. off-target/promiscuous compounds). Patent mentions across the top 20 by phase: 202,383 (via chembl_molecule»patent_compound — counts attach to the compound, not the gene–compound relationship, so off-target/promiscuous molecules can dominate).

Molecule	Name	Phase	Patents
CHEMBL499915	CARBENOXOLONE	4	3,947
CHEMBL140	CURCUMIN	3	93,882
CHEMBL297453	EPIGALOCATECHIN GALLATE	3	22,804
CHEMBL230006	ENOXOLONE	2	24,361
CHEMBL441687	GLYCYRRHIZIN	2	57,389

PharmGKB: 1 entry (VIP=true, CPIC=false)

GtoPdb / IUPHAR curated pharmacology

(IUPHAR/BPS Guide to Pharmacology — expert-curated)

Target class: enzyme — 1.-.-.- Oxidoreductases

Most potent curated ligand interactions (1 total), top 1:

Ligand	Action	Affinity	Parameter
enoxolone	Inhibition	8.92	pIC50

Binding affinities (BindingDB)

64 measured of 80 human assays (80 total across all organisms); most potent 50 below. Values come from heterogeneous assays and are not directly comparable.

Ligand	Measure	Value	Patent
4-[[2-[3-methyl-1,1-dioxo-6-(2,4,6-trichlorophenyl)-1,2,6-thiadiazinan-2-yl]acetyl]amino]adamantane-1-carboxamide	IC50	0.1 nM	US-9073906: Sulfamide derivative having an adamantyl group and its pharmaceutically acceptable salt
4-[[2-[1,1-dioxo-6-(2,4,6-trichlorophenyl)-1,2,6-thiadiazinan-2-yl]acetyl]amino]adamantane-1-carboxamide	IC50	0.2 nM	US-9073906: Sulfamide derivative having an adamantyl group and its pharmaceutically acceptable salt
4-[[2-[1,1-dioxo-7-(2,4,6-trichlorophenyl)-1,2,7-thiadiazepan-2-yl]acetyl]amino]adamantane-1-carboxamide	IC50	0.4 nM	US-9073906: Sulfamide derivative having an adamantyl group and its pharmaceutically acceptable salt
spiro-carboxamide scaffold, 13	IC50	0.5 nM
4-[[2-[methyl-[methyl-(2,4,6-trichlorophenyl)sulfamoyl]amino]acetyl]amino]adamantane-1-carboxamide	IC50	0.8 nM	US-9073906: Sulfamide derivative having an adamantyl group and its pharmaceutically acceptable salt
4-[[2-[4-methyl-1,1-dioxo-6-(2,4,6-trichlorophenyl)-1,2,6-thiadiazinan-2-yl]acetyl]amino]adamantane-1-carboxamide	IC50	1 nM	US-9073906: Sulfamide derivative having an adamantyl group and its pharmaceutically acceptable salt
4-[[2-[(4R)-6-[2,6-dichloro-4-(trifluoromethyl)phenyl]-4-methyl-1,1-dioxo-1,2,6-thiadiazinan-2-yl]acetyl]amino]adamantane-1-carboxamide	IC50	1.3 nM	US-9073906: Sulfamide derivative having an adamantyl group and its pharmaceutically acceptable salt
4-[[2-[6-(3-fluorophenyl)-1,1-dioxo-1,2,6-thiadiazinan-2-yl]acetyl]amino]adamantane-1-carboxamide	IC50	3 nM	US-9073906: Sulfamide derivative having an adamantyl group and its pharmaceutically acceptable salt
2-(hexahydro-2,5-methanopentalen-3a(1H)-ylamino)-1-thia-3-azaspiro[4.4]non-2-en-4-one	KI	3 nM
4-[[2-[6-[2,6-dichloro-4-(trifluoromethyl)phenyl]-4-methyl-1,1-dioxo-1,2,6-thiadiazinan-2-yl]acetyl]amino]adamantane-1-carboxamide	IC50	4.8 nM	US-9073906: Sulfamide derivative having an adamantyl group and its pharmaceutically acceptable salt
(1R,3R,4S,7S)-4-(2-methyl-2-phenoxypropanamido)adamantane-1-carboxamide	IC50	5 nM
4-[[2-[6,6-dioxo-7-(2,4,6-trichlorophenyl)-6lambda6-thia-5,7-diazaspiro[2.5]octan-5-yl]acetyl]amino]adamantane-1-carboxamide	IC50	5 nM	US-9073906: Sulfamide derivative having an adamantyl group and its pharmaceutically acceptable salt
4-[[2-[4,4-dimethyl-1,1-dioxo-6-(2,4,6-trichlorophenyl)-1,2,6-thiadiazinan-2-yl]acetyl]amino]adamantane-1-carboxamide	IC50	5 nM	US-9073906: Sulfamide derivative having an adamantyl group and its pharmaceutically acceptable salt
(1R,3R,4S,7S)-4-[2-(4-chlorophenoxy)-2-methylpropanamido]adamantane-1-carboxamide	IC50	6 nM
(1R,3R,4S,7S)-4-[2-(4-methoxyphenoxy)-2-methylpropanamido]adamantane-1-carboxamide	IC50	6 nM
spiro-carboxamide scaffold, 6	IC50	6 nM
(1R,3R,4S,7S)-4-[2-(2-chlorophenoxy)-2-methylpropanamido]adamantane-1-carboxylic acid	IC50	8 nM
2-(4-chlorophenoxy)-N-[(1R,2S,5R,7S)-5-(hydroxymethyl)adamantan-2-yl]-2-methylpropanamide	IC50	9 nM
2-(2-chloro-4-fluorophenoxy)-2-methyl-N-[(1R,2S,5R,7S)-5-(1H-1,2,3,4-tetrazol-5-yl)adamantan-2-yl]propanamide	IC50	11 nM
N-[(1R,2S,5R,7S)-5-[(carbamoylmethyl)carbamoyl]adamantan-2-yl]-2-(4-chlorophenoxy)-2-methylpropanamide	IC50	12 nM
N-(2-adamantyl)-2-(1,1-dioxo-6-phenyl-1,2,6-thiadiazinan-2-yl)acetamide	IC50	12 nM	US-9073906: Sulfamide derivative having an adamantyl group and its pharmaceutically acceptable salt
2-(4-chlorophenoxy)-2-methyl-N-[(1R,2S,5R,7S)-5-{[(methylcarbamoyl)amino]carbonyl}adamantan-2-yl]propanamide	IC50	13 nM
5-ethyl-5-methyl-2-{tricyclo[3.3.1.0^{3,7}]nonan-3-ylamino}-4,5-dihydro-1,3-thiazol-4-one	KI	13 nM
5,5-diethyl-2-{tricyclo[3.3.1.0^{3,7}]nonan-3-ylamino}-4,5-dihydro-1,3-thiazol-4-one	KI	13 nM
4-[[2-[6-(2-fluorophenyl)-1,1-dioxo-1,2,6-thiadiazinan-2-yl]acetyl]amino]adamantane-1-carboxamide	IC50	14 nM	US-9073906: Sulfamide derivative having an adamantyl group and its pharmaceutically acceptable salt
4-[[2-[4-methylidene-1,1-dioxo-6-(2,4,6-trichlorophenyl)-1,2,6-thiadiazinan-2-yl]acetyl]amino]adamantane-1-carboxamide	IC50	14 nM	US-9073906: Sulfamide derivative having an adamantyl group and its pharmaceutically acceptable salt
2-(cyclooctylamino)-1-thia-3-azaspiro[4.4]non-2-en-4-one	KI	14 nM
(1R,3R,4S,7S)-4-[2-(3-chlorophenoxy)-2-methylpropanamido]adamantane-1-carboxylic acid	IC50	15 nM
4-({[(1R,3R,4S,7S)-4-[2-(4-chlorophenoxy)-2-methylpropanamido]adamantan-1-yl]formamido}methyl)benzoic acid	IC50	15 nM
(1R,3R,4S,7S)-4-[2-(4-chlorophenoxy)-2-methylpropanamido]-N-{[4-(1H-1,2,3,4-tetrazol-5-yl)phenyl]methyl}adamantane-1-carboxamide	IC50	16 nM
4-[[2-(1,1-dioxo-6-phenyl-1,2,6-thiadiazinan-2-yl)acetyl]amino]adamantane-1-carboxamide	IC50	17 nM	US-9073906: Sulfamide derivative having an adamantyl group and its pharmaceutically acceptable salt
4-[[2-[1,1-dioxo-6-(2,4,6-trifluorophenyl)-1,2,6-thiadiazinan-2-yl]acetyl]amino]adamantane-1-carboxamide	IC50	20 nM	US-9073906: Sulfamide derivative having an adamantyl group and its pharmaceutically acceptable salt
(1R,3R,4S,7S)-4-[2-(4-chlorophenoxy)-2-methylpropanamido]adamantane-1-carboxylic acid	IC50	22 nM
spiro-carboxamide scaffold, 5	IC50	22 nM
(1R,3R,4S,7S)-4-[2-(4-chlorophenoxy)-2-methylpropanamido]-N-{[4-(methanesulfonylcarbamoyl)phenyl]methyl}adamantane-1-carboxamide	IC50	25 nM
(1R,3R,4S,7S)-4-[2-(4-chlorophenoxy)-2-methylpropanamido]-N-(pyridin-4-ylmethyl)adamantane-1-carboxamide	IC50	25 nM
spiro-carboxamide scaffold, 3	IC50	25 nM
2-(cyclooctylamino)-5,5-diethyl-4,5-dihydro-1,3-thiazol-4-one	KI	26 nM
(1R,3R,4S,7S)-4-[2-(4-chlorophenoxy)-2-methylpropanamido]-N-(1,3-thiazol-5-ylmethyl)adamantane-1-carboxamide	IC50	27 nM
2-(cyclooctylamino)-5-methyl-5-propyl-4,5-dihydro-1,3-thiazol-4-one	KI	28 nM
2-(cycloheptylamino)-5-methyl-5-propyl-4,5-dihydro-1,3-thiazol-4-one	KI	32 nM
(1R,3R,4S,7S)-4-(2-methyl-2-phenoxypropanamido)adamantane-1-carboxylic acid	IC50	39 nM
2-(cyclooctylamino)-5-ethyl-5-methyl-4,5-dihydro-1,3-thiazol-4-one	KI	47 nM
(1R,3R,4S,7S)-4-[2-(4-chlorophenoxy)-2-methylpropanamido]-N-[(4-sulfamoylphenyl)methyl]adamantane-1-carboxamide	IC50	51 nM
2-{bicyclo[2.2.1]heptan-1-ylamino}-5-ethyl-5-methyl-4,5-dihydro-1,3-thiazol-4-one	KI	73 nM
4-[[2-[6-(4-fluorophenyl)-1,1-dioxo-1,2,6-thiadiazinan-2-yl]acetyl]amino]adamantane-1-carboxamide	IC50	79 nM	US-9073906: Sulfamide derivative having an adamantyl group and its pharmaceutically acceptable salt
2-(cycloheptylamino)-5-ethyl-5-methyl-4,5-dihydro-1,3-thiazol-4-one	KI	82 nM
(1R,3R,4S,7S)-4-[2-(2-chlorophenoxy)-2-methylpropanamido]-N-methanesulfonyladamantane-1-carboxamide	IC50	96 nM
CHEMBL4160328	IC50	100 nM
2-{[(1R,3R,4S,7S)-4-[2-(4-chlorophenoxy)-2-methylpropanamido]adamantan-1-yl]methoxy}acetic acid	IC50	110 nM

ChEMBL bioactivities

121 potent at pChembl≥5 of 180 total, top 50 by pChembl (potency: 10 = 0.1 nM, 6 = 1 µM).

pChembl	Type	Value	Unit	Molecule
9.40	IC50	0.4	nM	GLYCYRRHIZIN
9.15	IC50	0.7	nM	GLYCYRRHIZIN
9.00	EC50	1	nM	GLYCYRRHIZIN
9.00	IC50	1	nM	GLYCYRRHIZIN
8.92	IC50	1.2	nM	ENOXOLONE
8.91	IC50	1.22	nM	ENOXOLONE
8.89	IC50	1.3	nM	ENOXOLONE
8.54	IC50	2.9	nM	CHEMBL1269273
8.52	IC50	3	nM	CHEMBL373257
8.31	IC50	4.9	nM	CHEMBL1271410
8.12	IC50	7.5	nM	CHEMBL1761313
8.00	IC50	10	nM	CHEMBL597481
7.96	IC50	11	nM	CHEMBL1689172
7.96	IC50	11	nM	CHEMBL1689280
7.84	IC50	14.5	nM	CHEMBL1269877
7.82	IC50	15	nM	CHEMBL1689282
7.77	IC50	17	nM	CHEMBL1689283
7.70	IC50	20	nM	CHEMBL384650
7.52	IC50	30.4	nM	CHEMBL2391969
7.51	IC50	31.2	nM	CHEMBL1761321
7.48	IC50	33	nM	CHEMBL1689279
7.35	IC50	45	nM	CHEMBL1689284
7.22	IC50	60	nM	CHEMBL425772
7.21	IC50	61.1	nM	CHEMBL1270688
7.00	IC50	100	nM	CHEMBL4160328
7.00	IC50	100	nM	CHEMBL4170932
6.98	IC50	104	nM	CHEMBL1689173
6.91	IC50	122	nM	CHEMBL1271303
6.77	IC50	170	nM	CARBENOXOLONE
6.75	IC50	180	nM	CHEMBL200513
6.74	IC50	183	nM	CHEMBL200513
6.71	IC50	194	nM	CHEMBL1689277
6.70	IC50	201	nM	ACETOXOLONE
6.67	IC50	216	nM	CHEMBL256090
6.64	IC50	228	nM	CHEMBL372768
6.59	IC50	257	nM	ENOXOLONE
6.57	IC50	268	nM	CHEMBL1270589
6.55	IC50	280	nM	CHEMBL382614
6.54	IC50	290	nM	CHEMBL1761135
6.48	IC50	329	nM	CHEMBL493512
6.42	IC50	380	nM	CHEMBL240269
6.41	IC50	386	nM	CHEMBL1911698
6.40	IC50	400	nM	CALONCOBIC ACID B
6.40	IC50	400	nM	CHEMBL1563246
6.34	IC50	458	nM	CHEMBL1270093
6.34	IC50	460	nM	CHEMBL1761142
6.31	IC50	490	nM	11BETA-HYDROXYPROGESTERONE
6.30	IC50	503	nM	CHEMBL256515
6.29	IC50	510	nM	CHEMBL597063
6.28	IC50	530	nM	CHEMBL240053

PubChem BioAssay actives

130 with measured affinity, of 1147 total; 50 most potent distinct compounds. Largely complementary to BindingDB; screening values are coarse (µM, 4 dp), so sub-nM hits tie at the floor.

Compound	Assay	Type	Value	Unit
Glycyrrhizin	664592: Inhibition of human 11beta-HSD2 expressed in HEK293 cells assessed as conversion of [3H]cortisone into [3H]cortisol by scintillation proximity assay	ic50	0.0004	uM
(2S,4aS,6aR,6aS,6bR,8aR,10S,12aS,14bR)-10-hydroxy-2,4a,6a,6b,9,9,12a-heptamethyl-13-oxo-3,4,5,6,6a,7,8,8a,10,11,12,14b-dodecahydro-1H-picene-2-carboxylic acid	1202733: Inhibition of human 11beta-HSD2 overexpressed in microsomal fraction of HEK293 cells using [3H]-cortisol as substrate by scintillation proximity assay in presence of NAD+	ic50	0.0012	uM
[(3S,4aR,6aR,6bS,8aS,11S,12aR,14aR,14bS)-11-[hydroxy(methyl)carbamoyl]-4,4,6a,6b,8a,11,14b-heptamethyl-14-oxo-2,3,4a,5,6,7,8,9,10,12,12a,14a-dodecahydro-1H-picen-3-yl] acetate	526982: Inhibition of human recombinant 11beta-HSD2 expressed in HEK293 cells assessed as conversion of [1,2,6,7-3H]-cortisol to cortisone by scintillation counting	ic50	0.0029	uM
3-(4-fluorophenyl)-5-[4-[4-methyl-5-[2-(trifluoromethyl)phenyl]-1,2,4-triazol-3-yl]-1-bicyclo[2.2.2]octanyl]-1,2,4-oxadiazole	753396: Inhibition of human microsomal 11beta-HSD2 assessed as inhibition of conversion of radiolabeled cortisone to radiolabeled cortisol by cell-based assay	ic50	0.0030	uM
(2S,4aS,6aR,6aS,6bR,8aR,10R,12aS,14bR)-10-(methoxyamino)-2,4a,6a,6b,9,9,12a-heptamethyl-13-oxo-3,4,5,6,6a,7,8,8a,10,11,12,14b-dodecahydro-1H-picene-2-carboxylic acid;hydrochloride	526982: Inhibition of human recombinant 11beta-HSD2 expressed in HEK293 cells assessed as conversion of [1,2,6,7-3H]-cortisol to cortisone by scintillation counting	ic50	0.0049	uM
3-[4-(2-ethylsulfonylethyl)-1-bicyclo[2.2.2]octanyl]-4-methyl-5-[2-(trifluoromethyl)phenyl]-1,2,4-triazole	753396: Inhibition of human microsomal 11beta-HSD2 assessed as inhibition of conversion of radiolabeled cortisone to radiolabeled cortisol by cell-based assay	ic50	0.0075	uM
2-[1’-(2-adamantylcarbamoyl)-6-methylspiro[1,2-dihydroindene-3,4’-piperidine]-1-yl]acetic acid	458825: Inhibition of 11beta-HSD2	ic50	0.0100	uM
(2S,4aS,6aR,6aS,6bR,8aR,10S,12aS,14bR)-2,4a,6a,6b,9,9,12a-heptamethyl-13-oxo-10-[(5-oxo-4H-1,2,4-oxadiazol-3-yl)oxy]-3,4,5,6,6a,7,8,8a,10,11,12,14b-dodecahydro-1H-picene-2-carboxylic acid	587116: Inhibition of human 11beta-HSD2 expressed in HEK293 cells assessed as conversion of [1,2,6,7-[3H]cortisol to cortisone after 10 mins by scintillation counting	ic50	0.0110	uM
(1R,2S,5S,8S,10R,14R,15S,21R)-N-hydroxy-N,1,2,5,8,15,20,20-octamethyl-13,18-dioxo-19-azapentacyclo[12.9.0.02,11.05,10.015,21]tricos-11-ene-8-carboxamide	587116: Inhibition of human 11beta-HSD2 expressed in HEK293 cells assessed as conversion of [1,2,6,7-[3H]cortisol to cortisone after 10 mins by scintillation counting	ic50	0.0110	uM
(2S,4aS,6aR,6aS,6bR,8aR,10S,12aS,14bR)-10-(methoxyamino)-2,4a,6a,6b,9,9,12a-heptamethyl-13-oxo-3,4,5,6,6a,7,8,8a,10,11,12,14b-dodecahydro-1H-picene-2-carboxylic acid;hydrochloride	526982: Inhibition of human recombinant 11beta-HSD2 expressed in HEK293 cells assessed as conversion of [1,2,6,7-3H]-cortisol to cortisone by scintillation counting	ic50	0.0145	uM
(2S,4aS,6aR,6aS,6bR,8aR,10S,12aS,14bR)-N-hydroxy-N,2,4a,6a,6b,9,9,12a-octamethyl-13-oxo-10-[(5-oxo-4H-1,2,4-oxadiazol-3-yl)oxy]-3,4,5,6,6a,7,8,8a,10,11,12,14b-dodecahydro-1H-picene-2-carboxamide	587116: Inhibition of human 11beta-HSD2 expressed in HEK293 cells assessed as conversion of [1,2,6,7-[3H]cortisol to cortisone after 10 mins by scintillation counting	ic50	0.0150	uM
[(2S,4aS,6aR,6aS,6bR,8aR,10S,12aS,14bR)-10-hydroxy-2,4a,6a,6b,9,9,12a-heptamethyl-13-oxo-3,4,5,6,6a,7,8,8a,10,11,12,14b-dodecahydro-1H-picen-2-yl]urea	587116: Inhibition of human 11beta-HSD2 expressed in HEK293 cells assessed as conversion of [1,2,6,7-[3H]cortisol to cortisone after 10 mins by scintillation counting	ic50	0.0170	uM
6-[(1-cycloheptyl-4,4-dimethyl-5-oxopyrrolidin-3-yl)methoxy]pyridine-3-carbonitrile	276076: Inhibition of human 11beta-HSD2	ic50	0.0200	uM
5-(1,1-difluoroethyl)-3-[4-[4-methyl-5-[2-(trifluoromethyl)phenyl]-1,2,4-triazol-3-yl]-1-bicyclo[2.2.2]octanyl]-1,2,4-oxadiazole	753396: Inhibition of human microsomal 11beta-HSD2 assessed as inhibition of conversion of radiolabeled cortisone to radiolabeled cortisol by cell-based assay	ic50	0.0304	uM
3-[4-(ethylsulfonylmethyl)-1-bicyclo[2.2.2]octanyl]-4-methyl-5-[2-(trifluoromethyl)phenyl]-1,2,4-triazole	753396: Inhibition of human microsomal 11beta-HSD2 assessed as inhibition of conversion of radiolabeled cortisone to radiolabeled cortisol by cell-based assay	ic50	0.0312	uM
[(1R,2S,5S,8S,10R,14R,15S,21R)-1,2,5,8,15,20,20-heptamethyl-13,18-dioxo-19-azapentacyclo[12.9.0.02,11.05,10.015,21]tricos-11-en-8-yl]urea	587116: Inhibition of human 11beta-HSD2 expressed in HEK293 cells assessed as conversion of [1,2,6,7-[3H]cortisol to cortisone after 10 mins by scintillation counting	ic50	0.0330	uM
[(2S,4aS,6aR,6aS,6bR,8aR,12aS,14bR)-2,4a,6a,6b,9,9,12a-heptamethyl-10,13-dioxo-1,3,4,5,6,6a,7,8,8a,11,12,14b-dodecahydropicen-2-yl]urea	587116: Inhibition of human 11beta-HSD2 expressed in HEK293 cells assessed as conversion of [1,2,6,7-[3H]cortisol to cortisone after 10 mins by scintillation counting	ic50	0.0450	uM
(2S,4aS,6aR,6aS,6bR,8aR,10S,12aS,14bR)-10-amino-2,4a,6a,6b,9,9,12a-heptamethyl-13-oxo-3,4,5,6,6a,7,8,8a,10,11,12,14b-dodecahydro-1H-picene-2-carboxylic acid	265990: Inhibition of human recombinant 11-beta-HSD2 expressed in HEK293 cells	ic50	0.0600	uM
[(3S,4aR,6aR,6bS,8aS,11S,12aR,14aR,14bS)-11-(hydroxycarbamoyl)-4,4,6a,6b,8a,11,14b-heptamethyl-14-oxo-2,3,4a,5,6,7,8,9,10,12,12a,14a-dodecahydro-1H-picen-3-yl] acetate	526982: Inhibition of human recombinant 11beta-HSD2 expressed in HEK293 cells assessed as conversion of [1,2,6,7-3H]-cortisol to cortisone by scintillation counting	ic50	0.0611	uM
4-azatetracyclo[5.3.2.02,6.08,10]dodecan-4-yl(cyclohexyl)methanone	1501003: Inhibition of human full-length 11beta-HSD2 expressed in HEK293 cells using cortisol as substrate after 2 hrs by LC-MS analysis	ic50	0.1000	uM
4-azatricyclo[5.2.2.02,6]undecan-4-yl(cyclohexyl)methanone	1501003: Inhibition of human full-length 11beta-HSD2 expressed in HEK293 cells using cortisol as substrate after 2 hrs by LC-MS analysis	ic50	0.1000	uM
4-azatricyclo[5.2.1.02,6]decan-4-yl(cyclohexyl)methanone	1501003: Inhibition of human full-length 11beta-HSD2 expressed in HEK293 cells using cortisol as substrate after 2 hrs by LC-MS analysis	ic50	0.1000	uM
4-azatricyclo[5.2.1.02,6]dec-8-en-4-yl(cyclohexyl)methanone	1501003: Inhibition of human full-length 11beta-HSD2 expressed in HEK293 cells using cortisol as substrate after 2 hrs by LC-MS analysis	ic50	0.1000	uM
4-azatricyclo[5.2.2.02,6]undec-8-en-4-yl(cyclohexyl)methanone	1501003: Inhibition of human full-length 11beta-HSD2 expressed in HEK293 cells using cortisol as substrate after 2 hrs by LC-MS analysis	ic50	0.1000	uM
[(3S,4aR,6aR,6bS,8aS,11S,12aR,14aR,14bS)-11-(carbamoylamino)-4,4,6a,6b,8a,11,14b-heptamethyl-14-oxo-2,3,4a,5,6,7,8,9,10,12,12a,14a-dodecahydro-1H-picen-3-yl] acetate	587116: Inhibition of human 11beta-HSD2 expressed in HEK293 cells assessed as conversion of [1,2,6,7-[3H]cortisol to cortisone after 10 mins by scintillation counting	ic50	0.1040	uM
(2S,4aS,6aR,6aS,6bR,8aR,10S,12aS,14bR)-N,10-dihydroxy-2,4a,6a,6b,9,9,12a-heptamethyl-13-oxo-3,4,5,6,6a,7,8,8a,10,11,12,14b-dodecahydro-1H-picene-2-carboxamide	526982: Inhibition of human recombinant 11beta-HSD2 expressed in HEK293 cells assessed as conversion of [1,2,6,7-3H]-cortisol to cortisone by scintillation counting	ic50	0.1220	uM
(2S,4aS,6aR,6aS,6bR,8aR,10S,12aS,14bR)-10-(3-carboxypropanoyloxy)-2,4a,6a,6b,9,9,12a-heptamethyl-13-oxo-3,4,5,6,6a,7,8,8a,10,11,12,14b-dodecahydro-1H-picene-2-carboxylic acid	1516424: Inhibition of 11beta-HSD2 (unknown origin) expressed in HEK293 cells using cortisone as substrate measured after 2 hrs in presence of NAD+ by HTRF assay	ic50	0.1700	uM
3-(4-pentyl-1-bicyclo[2.2.2]octanyl)-5,6,7,8,9,10-hexahydro-[1,2,4]triazolo[4,3-a]azocine	590789: Inhibition of human 11beta-HSD2 expressed in CHO-K1 cells assessed as conversion of [3H]-cortisol to [3H]-cortisone by scintillation proximity assay	ic50	0.1800	uM
[(3S,4aR,6aR,6bS,8aS,11S,12aR,14aR,14bS)-4,4,6a,6b,8a,11,14b-heptamethyl-14-oxo-11-(trifluoromethylsulfonylcarbamoylamino)-2,3,4a,5,6,7,8,9,10,12,12a,14a-dodecahydro-1H-picen-3-yl] acetate	587116: Inhibition of human 11beta-HSD2 expressed in HEK293 cells assessed as conversion of [1,2,6,7-[3H]cortisol to cortisone after 10 mins by scintillation counting	ic50	0.1940	uM
(2S,4aS,6aR,6aS,6bR,8aR,10S,12aS,14bR)-10-acetyloxy-2,4a,6a,6b,9,9,12a-heptamethyl-13-oxo-3,4,5,6,6a,7,8,8a,10,11,12,14b-dodecahydro-1H-picene-2-carboxylic acid	265990: Inhibition of human recombinant 11-beta-HSD2 expressed in HEK293 cells	ic50	0.2010	uM
3-[1-(4-methylphenyl)cyclohexyl]-5,6,7,8,9,10-hexahydro-[1,2,4]triazolo[4,3-a]azocine	332064: Inhibition of human 11-beta-HSD2 by SPA assay	ic50	0.2160	uM
3-(4-chlorophenyl)-5-[4-(5,6,7,8,9,10-hexahydro-[1,2,4]triazolo[4,3-a]azocin-3-yl)-1-bicyclo[2.2.2]octanyl]-1,2,4-oxadiazole	257372: Inhibitory activity against human 11beta-HSD2	ic50	0.2280	uM
(2S,4aS,6aR,6aS,6bR,8aR,10E,12aS,14bR)-10-methoxyimino-2,4a,6a,6b,9,9,12a-heptamethyl-13-oxo-1,3,4,5,6,6a,7,8,8a,11,12,14b-dodecahydropicene-2-carboxylic acid	526982: Inhibition of human recombinant 11beta-HSD2 expressed in HEK293 cells assessed as conversion of [1,2,6,7-3H]-cortisol to cortisone by scintillation counting	ic50	0.2680	uM
2-[[(3S,4aR,6aR,6bS,8aS,11S,12aR,14aR,14bS)-11-methoxycarbonyl-4,4,6a,6b,8a,11,14b-heptamethyl-14-oxo-2,3,4a,5,6,7,8,9,10,12,12a,14a-dodecahydro-1H-picen-3-yl]oxy]benzoic acid	265990: Inhibition of human recombinant 11-beta-HSD2 expressed in HEK293 cells	ic50	0.2800	uM
5-[4-(5,6,7,8,9,10-hexahydro-[1,2,4]triazolo[4,3-a]azocin-3-yl)-1-bicyclo[2.2.2]octanyl]pentan-2-ol	590789: Inhibition of human 11beta-HSD2 expressed in CHO-K1 cells assessed as conversion of [3H]-cortisol to [3H]-cortisone by scintillation proximity assay	ic50	0.2900	uM
(2S,4aS,6aR,6aS,6bR,8aR,12aS,14bR)-2,4a,6a,6b,9,9,12a-heptamethyl-10,13-dioxo-1,3,4,5,6,6a,7,8,8a,11,12,14b-dodecahydropicene-2-carboxylic acid	526982: Inhibition of human recombinant 11beta-HSD2 expressed in HEK293 cells assessed as conversion of [1,2,6,7-3H]-cortisol to cortisone by scintillation counting	ic50	0.3290	uM
5-cyclopentyl-2-(2-fluorophenyl)imino-1,3-thiazolidin-4-one	302632: Inhibition of human 11-beta-HSD2 by SPA	ic50	0.3800	uM
4-benzylsulfanyl-2-oxo-5,6-dihydro-3H-benzo[f]isoquinoline-1-carbonitrile	626064: Inhibition of 11beta-HSD2	ic50	0.3860	uM
(1S,3R,6S,8R,11R,12R,15R,16R)-15-[(2R,5R)-5,6-dihydroxy-6-methylheptan-2-yl]-6-hydroxy-7,7,16-trimethylpentacyclo[9.7.0.01,3.03,8.012,16]octadecane-12-carboxylic acid	664592: Inhibition of human 11beta-HSD2 expressed in HEK293 cells assessed as conversion of [3H]cortisone into [3H]cortisol by scintillation proximity assay	ic50	0.4000	uM
(8S,9S,10R,11R,13S,14S,17S)-17-acetyl-11-hydroxy-10,13-dimethyl-1,2,6,7,8,9,11,12,14,15,16,17-dodecahydrocyclopenta[a]phenanthren-3-one	779927: Inhibition of human recombinant 11beta-HSD2 expressed in HEK293 cells assessed as inhibition of [1,2,6,7-3H]-cortisol to [3H]cortisone preincubated for 10 mins before substrate addition by scintillation counting	ic50	0.4000	uM
(2S,4aS,6aR,6aS,6bR,8aR,10S,12aS,14bR)-10-acetamido-2,4a,6a,6b,9,9,12a-heptamethyl-13-oxo-3,4,5,6,6a,7,8,8a,10,11,12,14b-dodecahydro-1H-picene-2-carboxylic acid	526982: Inhibition of human recombinant 11beta-HSD2 expressed in HEK293 cells assessed as conversion of [1,2,6,7-3H]-cortisol to cortisone by scintillation counting	ic50	0.4580	uM
3-[4-[(4-chlorophenoxy)methyl]-1-bicyclo[2.2.2]octanyl]-4-methyl-5-[2-(trifluoromethyl)phenyl]-1,2,4-triazole	590789: Inhibition of human 11beta-HSD2 expressed in CHO-K1 cells assessed as conversion of [3H]-cortisol to [3H]-cortisone by scintillation proximity assay	ic50	0.4600	uM
(8S,9S,10R,11S,13S,14S,17S)-17-acetyl-11-hydroxy-10,13-dimethyl-1,2,6,7,8,9,11,12,14,15,16,17-dodecahydrocyclopenta[a]phenanthren-3-one	779927: Inhibition of human recombinant 11beta-HSD2 expressed in HEK293 cells assessed as inhibition of [1,2,6,7-3H]-cortisol to [3H]cortisone preincubated for 10 mins before substrate addition by scintillation counting	ic50	0.4900	uM
3-[1-(4-methylphenyl)cyclopentyl]-5,6,7,8,9,10-hexahydro-[1,2,4]triazolo[4,3-a]azocine	332064: Inhibition of human 11-beta-HSD2 by SPA assay	ic50	0.5030	uM
2-[1’-(2-adamantylcarbamoyl)-7-methylspiro[1,2-dihydroindene-3,4’-piperidine]-1-yl]acetic acid	458825: Inhibition of 11beta-HSD2	ic50	0.5100	uM
5-cyclohexyl-2-(2-fluorophenyl)imino-1,3-thiazolidin-4-one	302632: Inhibition of human 11-beta-HSD2 by SPA	ic50	0.5300	uM
2-(2-chloro-4-fluorophenoxy)-2-methyl-N-[5-(2H-tetrazol-5-yl)-2-adamantyl]propanamide	305337: Inhibition of human 11beta-HSD2 by SPA	ic50	0.5500	uM
2-(2-chloro-4-fluorophenoxy)-2-methyl-N-[(1R)-5-(2H-tetrazol-5-yl)-2-adamantyl]propanamide	1797082: Human and Mouse 11beta-HSD1 SPA Assay from Article 10.1016/j.bmcl.2006.10.074: “Discovery of adamantane ethers as inhibitors of 11beta-HSD-1: Synthesis and biological evaluation.”	ic50	0.5500	uM
(3R)-4-[[2-(2-chlorophenoxy)-2-methylpropanoyl]amino]-N-methylsulfonyladamantane-1-carboxamide	1797082: Human and Mouse 11beta-HSD1 SPA Assay from Article 10.1016/j.bmcl.2006.10.074: “Discovery of adamantane ethers as inhibitors of 11beta-HSD-1: Synthesis and biological evaluation.”	ic50	0.5800	uM
4-[[2-(2-chlorophenoxy)-2-methylpropanoyl]amino]-N-methylsulfonyladamantane-1-carboxamide	305337: Inhibition of human 11beta-HSD2 by SPA	ic50	0.5800	uM

CTD chemical–gene interactions

143 total (human), top 30 by PubMed support.

Chemical	Actions (top 5)	PubMed papers
bisphenol A	affects expression, affects methylation, decreases activity, decreases expression, increases activity (+1 more)	7
Cadmium	decreases activity, decreases methylation, increases activity, affects reaction, decreases expression (+3 more)	6
Estradiol	affects binding, increases expression, affects cotreatment, decreases expression	5
Colforsin	decreases activity, decreases expression, decreases reaction, increases expression	5
Progesterone	decreases reaction, increases expression, affects cotreatment, decreases activity, decreases expression	5
Hydrocortisone	affects binding, increases metabolic processing, increases oxidation, increases chemical synthesis, decreases expression (+1 more)	4
Valproic Acid	decreases expression, affects cotreatment, increases expression	4
tributyltin	decreases reaction, increases activity, affects reaction, decreases activity, increases expression (+1 more)	3
Benzo(a)pyrene	affects cotreatment, increases expression, decreases expression, decreases reaction	3
Dexamethasone	increases metabolic processing, increases oxidation, decreases reaction, increases expression	3
Dithiothreitol	decreases reaction, increases activity, decreases activity	3
Thiram	decreases activity, decreases reaction, increases reaction, increases oxidation	3
Itraconazole	decreases activity	3
sodium arsenite	increases expression, decreases expression	2
perfluorooctanoic acid	decreases activity, decreases expression	2
triphenyltin	decreases activity	2
hydroxyitraconazole	decreases activity	2
posaconazole	decreases activity	2
entinostat	increases expression, affects cotreatment	2
Acetaminophen	increases expression, decreases expression	2
Caffeine	decreases expression, decreases reaction, decreases activity, affects reaction	2
Carbenoxolone	decreases activity	2
Cortisone	increases chemical synthesis, increases oxidation, decreases reaction	2
Glucocorticoids	decreases reaction, affects expression, increases activity, decreases activity	2
Leukotriene B4	increases activity, decreases activity, affects cotreatment, decreases expression, decreases reaction	2
Nickel	decreases expression	2
Masoprocol	affects cotreatment, decreases expression, decreases activity, increases reaction, decreases reaction (+2 more)	2
Testosterone	increases expression, decreases activity, decreases reaction, affects cotreatment	2
8-Bromo Cyclic Adenosine Monophosphate	increases expression, decreases expression, affects cotreatment	2
Mifepristone	increases activity, increases reaction, decreases activity, decreases reaction, decreases expression (+1 more)	2

ChEMBL screening assays

125 unique, capped per target: 120 binding, 5 admet

Representative assays (with source publication via chembl_document):

Assay ID	Type	Description	Source paper
CHEMBL1013113	Binding	Inhibition of 11betaHSD2 at 100 uM by cell based assay	Piperazine sulfonamides as potent, selective, and orally available 11beta-hydroxysteroid dehydrogenase type 1 inhibitors with efficacy in the rat cortisone-induced hyperinsulinemia model. — J Med Chem
CHEMBL4016345	ADMET	Inhibition of human 11beta-HSD2 up to 30 uM	Discovery of Clinical Candidate 2-((2S,6S)-2-Phenyl-6-hydroxyadamantan-2-yl)-1-(3’-hydroxyazetidin-1-yl)ethanone [BMS-816336], an Orally Active Novel Selective 11β-Hydroxysteroid Dehydrogenase Type 1 Inhibitor. — J Med Chem

Clinical trials (associated diseases)

4 trials via MONDO — disease-level, not drug-specific.

Trial	Phase	Status	Title
NCT00759525	PHASE2/PHASE3	COMPLETED	The Role of Mineralocorticoid Receptors in Vascular Function
NCT00474942	Not specified	COMPLETED	Natural History of Apparent Mineralocorticoid Excess Syndrome
NCT02939144	Not specified	COMPLETED	An Investigation Into the Effect of Liquorice Ingestion on the Salivary Cortisol to Cortisone Molar Ratio
NCT03655223	Not specified	ENROLLING_BY_INVITATION	Early Check: Expanded Screening in Newborns