Drug Information

Drug (ID: DG00580) and It's Reported Resistant Information

• Name: Bromocriptine
• Synonyms: Bromocriptine; Bromocryptine; 25614-03-3; Bromocriptin; Bromoergocryptine; Bromoergocriptine; Bromergocryptine; 2-Bromo-alpha-ergocryptine; Parlodel; 2-Bromo-alpha-ergokryptine; Bromocriptina; Bromocriptinum; 2-Bromo-alpha-ergokryptin; Bromocriptinum [INN-Latin]; Bromocriptina [INN-Spanish]; Bagren; Bromocriptine methanesulfonate; UNII-3A64E3G5ZO; CB-154; 2-Bromoergocryptine; Ergocryptine, 2-bromo-; 3A64E3G5ZO; CHEBI:3181; Ergotaman-3',6',18-trione, 2-bromo-12'-hydroxy-2'-(1-methylethyl)-5'-(2-methylpropyl)-, (5'alpha)-; Ergoset; Bromergon; CB 154; 22260-51-1; (5'alpha)-2-bromo-12'-hydroxy-2'-(1-methylethyl)-5'-(2-methylpropyl)-3',6',18-trioxoergotaman; 2-Bromo-.alpha.-ergocryptine; Bromocriptine (mesylate); C32H40BrN5O5; CCRIS 3244; NSC169774; EINECS 247-128-5; Bromocriptine (USAN/INN); SR-01000075356; Bromocriptine [USAN:INN:BAN]; NCGC00024584-03; 08Y; 2-Bromo-12'-hydroxy-2'-(1-methylethyl)-5'-alpha-(2-methylpropyl)ergotamin-3',6',18-trione; Bromocriptine+ (GTP-); Prestwick0_000121; Prestwick1_000121; Prestwick2_000121; Carboprost Methylate,(S); DSSTox_CID_2687; Biomol-NT_000005; CHEMBL493; GTPL35; (5'alpha)-2-bromo-12'-hydroxy-5'-isobutyl-2'-isopropyl-3',6',18-trioxoergotaman; DSSTox_RID_76692; DSSTox_GSID_22687; Lopac0_000171; SCHEMBL25297; (5'alpha)-2-bromo-12'-hydroxy-2'-(1-methylethyl)-5'-(2-methylpropyl)ergotaman-3',6',18-trione; BIDD:GT0464; SPBio_002101; BPBio1_001131; DTXSID1022687; SANDOZ 15-754; BDBM81993; Ergocryptine, 2-bromo- (8CI); Tox21_110907; PDSP2_001500; ZINC53683151; AKOS015961273; CCG-204266; DB01200; SDCCGSBI-0050159.P003; dioxooctahydro-2H-oxazolo[3,2-a]pyrrolo; NCGC00024584-04; NCGC00024584-05; NCGC00024584-07; NCGC00024584-09; (5'alpha)-2-bromo-12'-hydroxy-5'-(2-methylpropyl)-2'-(propan-2-yl)-3',6',18-trioxoergotaman; (6aR,9R)-5-Bromo-N-((2R,5S,10aS,10bS)-10b-hydroxy-5-isobutyl-2-isopropyl-3,6-dioxooctahydro-2H-oxazolo[3,2-a]pyrrolo[2,1-c]pyrazin-2-yl)-7-methyl-4,6,6a,7,8,9-hexahydroindolo[4,3-fg]quinoline-9-carboxamide; AC-13601; NCI60_001365; 10b-hydroxy-5-isobutyl-2-isopropyl-3,6-; CAS-25614-03-3; C06856; D03165; hexahydroindolo[4,3-fg]quinoline-9-carboxamide; Q413581; J-016067; SR-01000075356-5; (6aR,9R)-5-bromo-N-((2R,5S,10aS,10bS)-; [2,1-c]pyrazin-2-yl)-7-methyl-4,6,6a,7,8,9-; BRD-K14496212-001-01-1; BRD-K14496212-066-04-8; (4R,7R)-10-bromo-N-[(1S,2S,4R,7S)-2-hydroxy-7-(2-methylpropyl)-5,8-dioxo-4-(propan-2-yl)-3-oxa-6,9-diazatricyclo[7.3.0.0^{2,6}]dodecan-4-yl]-6-methyl-6,11-diazatetracyclo[7.6.1.0^{2,7}.0^{12,16}]hexadeca-1(16),2,9,12,14-pentaene-4-carboxamide; (5alpha,5'beta)-2-bromo-12'-hydroxy-5'-(2-methylpropyl)-3',6',18-trioxo-2'-(propan-2-yl)ergotaman; (6aR,9R)-5-bromo-N-[(1S,2S,4R,7S)-2-hydroxy-7-(2-methylpropyl)-5,8-dioxo-4-propan-2-yl-3-oxa-6,9-diazatricyclo[7.3.0.02,6]dodecan-4-yl]-7-methyl-6,6a,8,9-tetrahydro-4H-indolo[4,3-fg]quinoline-9-carboxamide; N-[(2R,5S,10aS,10bS)-10b-hydroxy-5-isobutyl-2-isopropyl-3,6-dioxo-8,9,10,10a-tetrahydro-5H-oxazolo[[ ]]pyrrolo[[ ]]pyrazin-2-yl]-bromo-methyl-[ ]carboxamide
• Indication:
  In total 1 Indication(s)
  Parkinson disease [ICD-11: 8A00]; Approved; [1]
• Drug Resistance Disease(s):
  Disease(s) with Clinically Reported Resistance for This Drug (1 diseases)
  Pituitary cancer [ICD-11: 2F37]; [1]
  Disease(s) with Resistance Information Discovered by Cell Line Test for This Drug (1 diseases)
  Pituitary cancer [ICD-11: 2F37]; [2]
• Target: Dopamine D2 receptor (D2R); DRD2_HUMAN; [1]
• Formula: C32H40BrN5O5
• IsoSMILES: CC(C)C[C@H]1C(=O)N2CCC[C@H]2[C@]3(N1C(=O)[C@](O3)(C(C)C)NC(=O)[C@H]4CN([C@@H]5CC6=C(NC7=CC=CC(=C67)C5=C4)Br)C)O
• InChI: 1S/C32H40BrN5O5/c1-16(2)12-24-29(40)37-11-7-10-25(37)32(42)38(24)30(41)31(43-32,17(3)4)35-28(39)18-13-20-19-8-6-9-22-26(19)21(27(33)34-22)14-23(20)36(5)15-18/h6,8-9,13,16-18,23-25,34,42H,7,10-12,14-15H2,1-5H3,(H,35,39)/t18-,23-,24+,25+,31-,32+/m1/s1
• InChIKey: OZVBMTJYIDMWIL-AYFBDAFISA-N
• PubChem CID: 31101
• ChEBI ID: CHEBI:3181
• TTD Drug ID: D06YFA
• VARIDT ID: DR00550
• DrugBank ID: DB01200

Type(s) of Resistant Mechanism of This Drug

  ADTT: Aberration of the Drug's Therapeutic Target

  EADR: Epigenetic Alteration of DNA, RNA or Protein

  RTDM: Regulation by the Disease Microenvironment

  UAPP: Unusual Activation of Pro-survival Pathway

Drug Resistance Data Categorized by Their Corresponding Diseases

ICD-02: Benign/in-situ/malignant neoplasm

Pituitary cancer [ICD-11: 2F37]

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Aberration of the Drug's Therapeutic Target (ADTT)

Key Molecule: Dopamine receptor D2 (DRD2) [3]

• Resistant Disease: Prolactin-secreting adenoma [ICD-11: 2F37.Y]
• Molecule Alteration: Expression; Down-regulation
• Experimental Note: Identified from the Human Clinical Data
• Mechanism Description: Generally, the effectiveness of BRC or CAB has been related to a decreased expression in DRs, as the expression of such receptors has been shown to correlate with responsiveness to therapy in lactotroph, somatotroph, corticotroph and in clinically nonfunctioning PitNET.

Epigenetic Alteration of DNA, RNA or Protein (EADR)

Key Molecule: hsa-miR-17-5p [4]

• Resistant Disease: Prolactin-secreting adenoma [ICD-11: 2F37.Y]
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Identified from the Human Clinical Data
• Cell Pathway Regulation: Cell proliferation; Activation; hsa05200
• In Vitro Model: C4-2 cells; Prostate; Homo sapiens (Human); CVCL_4782
• Experiment for Molecule Alteration: Solexa sequencing assay; qRT-PCR
• Experiment for Drug Resistance: CCK-8 assay
• Mechanism Description: Overexpression of mir-93 increased resistance to bromocriptine and cabergoline treatment.

Key Molecule: hsa-mir-126 [4]

• Resistant Disease: Prolactin-secreting adenoma [ICD-11: 2F37.Y]
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: KHM-5M cells; Pleural effusion; Homo sapiens (Human); CVCL_2975
• Experiment for Molecule Alteration: Solexa sequencing assay; qRT-PCR
• Experiment for Drug Resistance: Clinical diagnostic evaluation
• Mechanism Description: Hsa-mir-93, hsa-mir-17, hsa-mir-22*, hsa-mir-126*, hsa-mir-142-3p, hsa-mir-144*, hsa-mir-486-5p, hsa-mir-451, and hsa-mir-92a were up-regulated and hsa-mir-30a, hsa-mir-382, and hsa-mir-136 were down-regulated in bromocriptine-resistant prolactinomas in comparison with bromocriptine-sensitive prolactinomas.

Key Molecule: hsa-mir-136 [4]

• Resistant Disease: Prolactin-secreting adenoma [ICD-11: 2F37.Y]
• Molecule Alteration: Expression; Down-regulation
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: KHM-5M cells; Pleural effusion; Homo sapiens (Human); CVCL_2975
• Experiment for Molecule Alteration: Solexa sequencing assay; qRT-PCR
• Experiment for Drug Resistance: Clinical diagnostic evaluation
• Mechanism Description: Hsa-mir-93, hsa-mir-17, hsa-mir-22*, hsa-mir-126*, hsa-mir-142-3p, hsa-mir-144*, hsa-mir-486-5p, hsa-mir-451, and hsa-mir-92a were up-regulated and hsa-mir-30a, hsa-mir-382, and hsa-mir-136 were down-regulated in bromocriptine-resistant prolactinomas in comparison with bromocriptine-sensitive prolactinomas.

Key Molecule: hsa-miR-142-3p [4]

• Resistant Disease: Prolactin-secreting adenoma [ICD-11: 2F37.Y]
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: KHM-5M cells; Pleural effusion; Homo sapiens (Human); CVCL_2975
• Experiment for Molecule Alteration: Solexa sequencing assay; qRT-PCR
• Experiment for Drug Resistance: Clinical diagnostic evaluation
• Mechanism Description: Hsa-mir-93, hsa-mir-17, hsa-mir-22*, hsa-mir-126*, hsa-mir-142-3p, hsa-mir-144*, hsa-mir-486-5p, hsa-mir-451, and hsa-mir-92a were up-regulated and hsa-mir-30a, hsa-mir-382, and hsa-mir-136 were down-regulated in bromocriptine-resistant prolactinomas in comparison with bromocriptine-sensitive prolactinomas.

Key Molecule: hsa-mir-144 [4]

• Resistant Disease: Prolactin-secreting adenoma [ICD-11: 2F37.Y]
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: KHM-5M cells; Pleural effusion; Homo sapiens (Human); CVCL_2975
• Experiment for Molecule Alteration: Solexa sequencing assay; qRT-PCR
• Experiment for Drug Resistance: Clinical diagnostic evaluation
• Mechanism Description: Hsa-mir-93, hsa-mir-17, hsa-mir-22*, hsa-mir-126*, hsa-mir-142-3p, hsa-mir-144*, hsa-mir-486-5p, hsa-mir-451, and hsa-mir-92a were up-regulated and hsa-mir-30a, hsa-mir-382, and hsa-mir-136 were down-regulated in bromocriptine-resistant prolactinomas in comparison with bromocriptine-sensitive prolactinomas.

Key Molecule: hsa-mir-17 [4]

• Resistant Disease: Prolactin-secreting adenoma [ICD-11: 2F37.Y]
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: KHM-5M cells; Pleural effusion; Homo sapiens (Human); CVCL_2975
• Experiment for Molecule Alteration: Solexa sequencing assay; qRT-PCR
• Experiment for Drug Resistance: Clinical diagnostic evaluation
• Mechanism Description: Hsa-mir-93, hsa-mir-17, hsa-mir-22*, hsa-mir-126*, hsa-mir-142-3p, hsa-mir-144*, hsa-mir-486-5p, hsa-mir-451, and hsa-mir-92a were up-regulated and hsa-mir-30a, hsa-mir-382, and hsa-mir-136 were down-regulated in bromocriptine-resistant prolactinomas in comparison with bromocriptine-sensitive prolactinomas.

Key Molecule: hsa-mir-22 [4]

• Resistant Disease: Prolactin-secreting adenoma [ICD-11: 2F37.Y]
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: KHM-5M cells; Pleural effusion; Homo sapiens (Human); CVCL_2975
• Experiment for Molecule Alteration: Solexa sequencing assay; qRT-PCR
• Experiment for Drug Resistance: Clinical diagnostic evaluation
• Mechanism Description: Hsa-mir-93, hsa-mir-17, hsa-mir-22*, hsa-mir-126*, hsa-mir-142-3p, hsa-mir-144*, hsa-mir-486-5p, hsa-mir-451, and hsa-mir-92a were up-regulated and hsa-mir-30a, hsa-mir-382, and hsa-mir-136 were down-regulated in bromocriptine-resistant prolactinomas in comparison with bromocriptine-sensitive prolactinomas.

Key Molecule: hsa-mir-30a [4]

• Resistant Disease: Prolactin-secreting adenoma [ICD-11: 2F37.Y]
• Molecule Alteration: Expression; Down-regulation
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: KHM-5M cells; Pleural effusion; Homo sapiens (Human); CVCL_2975
• Experiment for Molecule Alteration: Solexa sequencing assay; qRT-PCR
• Experiment for Drug Resistance: Clinical diagnostic evaluation
• Mechanism Description: Hsa-mir-93, hsa-mir-17, hsa-mir-22*, hsa-mir-126*, hsa-mir-142-3p, hsa-mir-144*, hsa-mir-486-5p, hsa-mir-451, and hsa-mir-92a were up-regulated and hsa-mir-30a, hsa-mir-382, and hsa-mir-136 were down-regulated in bromocriptine-resistant prolactinomas in comparison with bromocriptine-sensitive prolactinomas.

Key Molecule: hsa-mir-382 [4]

• Resistant Disease: Prolactin-secreting adenoma [ICD-11: 2F37.Y]
• Molecule Alteration: Expression; Down-regulation
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: KHM-5M cells; Pleural effusion; Homo sapiens (Human); CVCL_2975
• Experiment for Molecule Alteration: Solexa sequencing assay; qRT-PCR
• Experiment for Drug Resistance: Clinical diagnostic evaluation
• Mechanism Description: Hsa-mir-93, hsa-mir-17, hsa-mir-22*, hsa-mir-126*, hsa-mir-142-3p, hsa-mir-144*, hsa-mir-486-5p, hsa-mir-451, and hsa-mir-92a were up-regulated and hsa-mir-30a, hsa-mir-382, and hsa-mir-136 were down-regulated in bromocriptine-resistant prolactinomas in comparison with bromocriptine-sensitive prolactinomas.

Key Molecule: hsa-mir-451 [4]

• Resistant Disease: Prolactin-secreting adenoma [ICD-11: 2F37.Y]
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: KHM-5M cells; Pleural effusion; Homo sapiens (Human); CVCL_2975
• Experiment for Molecule Alteration: Solexa sequencing assay; qRT-PCR
• Experiment for Drug Resistance: Clinical diagnostic evaluation
• Mechanism Description: Hsa-mir-93, hsa-mir-17, hsa-mir-22*, hsa-mir-126*, hsa-mir-142-3p, hsa-mir-144*, hsa-mir-486-5p, hsa-mir-451, and hsa-mir-92a were up-regulated and hsa-mir-30a, hsa-mir-382, and hsa-mir-136 were down-regulated in bromocriptine-resistant prolactinomas in comparison with bromocriptine-sensitive prolactinomas.

Key Molecule: hsa-miR-486-5p [4]

• Resistant Disease: Prolactin-secreting adenoma [ICD-11: 2F37.Y]
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: KHM-5M cells; Pleural effusion; Homo sapiens (Human); CVCL_2975
• Experiment for Molecule Alteration: Solexa sequencing assay; qRT-PCR
• Experiment for Drug Resistance: Clinical diagnostic evaluation
• Mechanism Description: Hsa-mir-93, hsa-mir-17, hsa-mir-22*, hsa-mir-126*, hsa-mir-142-3p, hsa-mir-144*, hsa-mir-486-5p, hsa-mir-451, and hsa-mir-92a were up-regulated and hsa-mir-30a, hsa-mir-382, and hsa-mir-136 were down-regulated in bromocriptine-resistant prolactinomas in comparison with bromocriptine-sensitive prolactinomas.

Key Molecule: Long non-protein coding RNA (lnc886) [4]

• Resistant Disease: Prolactin-secreting adenoma [ICD-11: 2F37.Y]
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: KHM-5M cells; Pleural effusion; Homo sapiens (Human); CVCL_2975
• Experiment for Molecule Alteration: Solexa sequencing assay; qRT-PCR
• Experiment for Drug Resistance: Clinical diagnostic evaluation
• Mechanism Description: Hsa-mir-93, hsa-mir-17, hsa-mir-22*, hsa-mir-126*, hsa-mir-142-3p, hsa-mir-144*, hsa-mir-486-5p, hsa-mir-451, and hsa-mir-92a were up-regulated and hsa-mir-30a, hsa-mir-382, and hsa-mir-136 were down-regulated in bromocriptine-resistant prolactinomas in comparison with bromocriptine-sensitive prolactinomas.

Key Molecule: hsa-mir-93 [4]

• Resistant Disease: Prolactin-secreting adenoma [ICD-11: 2F37.Y]
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: C4-2 cells; Prostate; Homo sapiens (Human); CVCL_4782
• In Vitro Model: KHM-5M cells; Pleural effusion; Homo sapiens (Human); CVCL_2975
• Experiment for Drug Resistance: Clinical diagnostic evaluation
• Mechanism Description: Hsa-mir-93, hsa-mir-17, hsa-mir-22*, hsa-mir-126*, hsa-mir-142-3p, hsa-mir-144*, hsa-mir-486-5p, hsa-mir-451, and hsa-mir-92a were up-regulated and hsa-mir-30a, hsa-mir-382, and hsa-mir-136 were down-regulated in bromocriptine-resistant prolactinomas in comparison with bromocriptine-sensitive prolactinomas.

Regulation by the Disease Microenvironment (RTDM)

Key Molecule: Mothers against decapentaplegic homolog 3 (SMAD3) [1]

• Resistant Disease: Prolactinomas [ICD-11: 2F37.2]
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Identified from the Human Clinical Data
• Cell Pathway Regulation: TGF-beta 1/Smad3 pathway; Activation; hsa04350
• In Vitro Model: HS27 cells; Bone; Homo sapiens (Human); CVCL_0E34
• In Vitro Model: MMQ cells; Pituitary gland; Rattus norvegicus (Rat); CVCL_2117
• Experiment for Molecule Alteration: Western blotting assay
• Experiment for Drug Resistance: CCK8 assay
• Mechanism Description: TGF-beta1 promotes the synthesis and secretion of collagen fibers in fibroblasts and that the TGF-beta1/Smad3 pathway is involved in the mechanism of prolactinoma resistance by increasing fibrosis through interactions with fibroblasts.

Key Molecule: Mothers against decapentaplegic homolog 4 (SMAD4) [1]

• Resistant Disease: Prolactinomas [ICD-11: 2F37.2]
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Identified from the Human Clinical Data
• Cell Pathway Regulation: TGF-beta 1/Smad3 pathway; Activation; hsa04350
• In Vitro Model: HS27 cells; Bone; Homo sapiens (Human); CVCL_0E34
• In Vitro Model: MMQ cells; Pituitary gland; Rattus norvegicus (Rat); CVCL_2117
• Experiment for Molecule Alteration: Western blotting assay
• Experiment for Drug Resistance: CCK8 assay
• Mechanism Description: TGF-beta1 promotes the synthesis and secretion of collagen fibers in fibroblasts and that the TGF-beta1/Smad3 pathway is involved in the mechanism of prolactinoma resistance by increasing fibrosis through interactions with fibroblasts.

Key Molecule: TSPY like 2 (TSPYL2) [1]

• Resistant Disease: Prolactinomas [ICD-11: 2F37.2]
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Identified from the Human Clinical Data
• Cell Pathway Regulation: TGF-beta 1/Smad3 pathway; Activation; hsa04350
• In Vitro Model: HS27 cells; Bone; Homo sapiens (Human); CVCL_0E34
• In Vitro Model: MMQ cells; Pituitary gland; Rattus norvegicus (Rat); CVCL_2117
• Experiment for Molecule Alteration: Western blotting assay
• Experiment for Drug Resistance: CCK8 assay
• Mechanism Description: TGF-beta1 promotes the synthesis and secretion of collagen fibers in fibroblasts and that the TGF-beta1/Smad3 pathway is involved in the mechanism of prolactinoma resistance by increasing fibrosis through interactions with fibroblasts.

Unusual Activation of Pro-survival Pathway (UAPP)

Key Molecule: Cyclin-dependent kinase inhibitor 1A (CDKN1A) [4]

• Resistant Disease: Prolactin-secreting adenoma [ICD-11: 2F37.Y]
• Molecule Alteration: Expression; Down-regulation
• Experimental Note: Identified from the Human Clinical Data
• Cell Pathway Regulation: Cell invasion; Activation; hsa05200
• Cell Pathway Regulation: Cell migration; Activation; hsa04670
• In Vitro Model: C4-2 cells; Prostate; Homo sapiens (Human); CVCL_4782
• Experiment for Molecule Alteration: Western blot analysis
• Experiment for Drug Resistance: CCK-8 assay
• Mechanism Description: Knockdown of mir-93 increased the sensitivity of MMQ cells to bromocriptine treatment, and these effects were abolished when p21 was knocked-down using siRNA.

Key Molecule: Androgen receptor (AR) [2]

• Resistant Disease: Prolactinomas [ICD-11: 2F37.2]
• Molecule Alteration: Expression; Up-regulation
• Experimental Note: Revealed Based on the Cell Line Data
• In Vitro Model: GH3 cells; Pituitary gland; Rattus norvegicus (Rat); CVCL_0273
• In Vitro Model: MMQ cells; Pituitary gland; Rattus norvegicus (Rat); CVCL_2117
• Experiment for Molecule Alteration: Western blot assay
• Experiment for Drug Resistance: Cell viability assay
• Mechanism Description: AR plays a crucial role in mediating DA resistance in PRL adenoma. Mechanistically, AR promotes cell proliferation and PRL secretion and confers drug resistance by transcriptionally regulating NRF2 expression to maintain redox homeostasis in PA cells. Finally, combining AR targeting agents with BRC shows promise as a therapeutic strategy for treating PRL adenomas.?Antioxid. Redox Signal.

References

• Ref 1: Role of TGF-Beta1/Smad3-mediated fibrosis in drug resistance mechanism of prolactinoma .Brain Res. 2018 Nov 1;1698:204-212. doi: 10.1016/j.brainres.2018.07.024. Epub 2018 Jul 27. 10.1016/j.brainres.2018.07.024
• Ref 2: Androgen Receptor Mediates Dopamine Agonist Resistance by Regulating Intracellular Reactive Oxygen Species in Prolactin-Secreting Pituitary Adenoma. Antioxid Redox Signal. 2025 Jun;42(16-18):954-972.
• Ref 3: Resistance to Dopamine Agonists in Pituitary Tumors: Molecular Mechanisms .Front Endocrinol (Lausanne). 2022 Jan 12;12:791633. doi: 10.3389/fendo.2021.791633. eCollection 2021. 10.3389/fendo.2021.791633
• Ref 4: MicroRNA expression profile of bromocriptine-resistant prolactinomas .Mol Cell Endocrinol. 2014 Sep;395(1-2):10-8. doi: 10.1016/j.mce.2014.07.014. Epub 2014 Jul 23. 10.1016/j.mce.2014.07.014