Drug Information

Drug (ID: DG01817) and It's Reported Resistant Information

• Name: Isoliquiritigenin
• Synonyms: Isoliquiritigenin; 961-29-5; 2',4,4'-Trihydroxychalcone; (E)-1-(2,4-dihydroxyphenyl)-3-(4-hydroxyphenyl)prop-2-en-1-one; 4,2',4'-Trihydroxychalcone; 6'-deoxychalcone; 2',4',4-Trihydroxychalcone; isoliquirtigenin; UNII-B9CTI9GB8F; C15H12O4; Chalcone, 2',4,4'-trihydroxy-; B9CTI9GB8F; 13745-20-5; 42'4'-trihydroxychalcone; 1-(2,4-Dihydroxyphenyl)-3-(4-hydroxyphenyl)-2-propen-1-one; (2E)-1-(2,4-dihydroxyphenyl)-3-(4-hydroxyphenyl)prop-2-en-1-one; 2-Propen-1-one, 1-(2,4-dihydroxyphenyl)-3-(4-hydroxyphenyl)-, (2E)-; Acrylophenone, 2',4'-dihydroxy-3-(p-hydroxyphenyl)-; CHEMBL129795; GU17; 1-(2,4-Dihydroxyphenyl)-3-(4-hydroxyphenyl)prop-2-en-1-one; CHEBI:310312; (E)-1-(2,4-Dihydroxyphenyl)-3-(4-hydroxyphenyl)-2-propen-1-one; trans-2',4,4'-trihydroxychalcone; 2-PROPEN-1-ONE, 1-(2,4-DIHYDROXYPHENYL)-3-(4-HYDROXYPHENYL)-; MFCD00075907; (E)-1-(2,4-Dihydroxy-phenyl)-3-(4-hydroxy-phenyl)-propenone; 1060-19-1; (E)-1-(2,4-dihydroxyphenyl)-3-(4-hydroxyphenyl)-2-propene-1-one; GU 17; GU-17; SMR000112969; CCRIS 7676; SR-01000075499; EINECS 237-316-5; BRN 1914295; Isoliquiritigen; iso-Liquiritigenin; ILTG; ISLQ; Isoliquiritigenin, powder; Spectrum5_000612; (2E)-1-(2,4-Dihydroxyphenyl)-3-(4-hydroxyphenyl)-2-propen-1-one; 2-Propen-1-one, 1-(2,4-dihydroxyphenyl)-3-(4-hydroxyphenyl)-, (E)-; Lopac0_000681; BSPBio_003411; 1-08-00-00707 (Beilstein Handbook Reference); MLS000438943; MLS002207240; MLS006010045; BIDD:ER0235; SCHEMBL161168; SPECTRUM1504200; cid_638278; MEGxp0_001326; 2',4,4'-Trihydroxy-Chalcone; DTXSID2022466; 2'',4'',4-trihydroxychalcone; 2'',4,4''-trihydroxychalcone; ACon1_000047; CHEBI:94010; BCPP000201; HMS2233H18; HMS3262I03; 2,4''-dihydroxy-4-hydroxychalcone; BCP02312; HY-N0102; ZINC3869608; Tox21_500681; BDBM50042944; CCG-40334; CMLD3_000056; LMPK12120096; s2404; 2',4,4'-Trihydroxychalcone, 97%; Isoliquiritigenin, analytical standard; AKOS001590146; BCP9000795; CS-1745; DB03285; KS-5256; LP00681; MCULE-1557671934; SDCCGMLS-0066751.P001; SDCCGSBI-0050660.P004; NCGC00090504-01; NCGC00090504-02; NCGC00090504-03; NCGC00090504-04; NCGC00090504-05; NCGC00090504-06; NCGC00090504-07; NCGC00090504-08; NCGC00090504-24; NCGC00261366-01; AC-33981; O271; EU-0100681; I0822; N1288; SW219658-1; C08650; I 3766; I11575; 961I295; A845551; NCGC00090504-04!2',4,4'-Trihydroxychalcone; 2',4'-Dihydroxy-3-(p-hydroxyphenyl)-Acrylophenone; Q-100904; Q3155537; SR-01000075499-1; SR-01000075499-5; BRD-K33583600-001-03-9; BRD-K33583600-001-04-7; 1-(2,4-Dihydroxy-phenyl)-3-(4-hydroxy-phenyl)-propenone; 1-(2,4-Dihydroxyphenyl)-3-(4-hydroxyphenyl)-prop-2-en-1-one; (E)-1-[2,4-bis(oxidanyl)phenyl]-3-(4-hydroxyphenyl)prop-2-en-1-one
• Drug Resistance Disease(s):
  Disease(s) with Resistance Information Validated by in-vivo Model for This Drug (1 diseases)
  Brain cancer [ICD-11: 2A00]; [1]
• Formula: 3
• IsoSMILES: C1=CC(=CC=C1/C=C/C(=O)C2=C(C=C(C=C2)O)O)O
• InChI: InChI=1S/C15H12O4/c16-11-4-1-10(2-5-11)3-8-14(18)13-7-6-12(17)9-15(13)19/h1-9,16-17,19H/b8-3+
• InChIKey: DXDRHHKMWQZJHT-FPYGCLRLSA-N
• PubChem CID: 638278
• DrugBank ID: DB03285

Type(s) of Resistant Mechanism of This Drug

  EADR: Epigenetic Alteration of DNA, RNA or Protein

  UAPP: Unusual Activation of Pro-survival Pathway

Drug Resistance Data Categorized by Their Corresponding Diseases

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

Brain cancer [ICD-11: 2A00]

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Epigenetic Alteration of DNA, RNA or Protein (EADR)

Key Molecule: Nuclear paraspeckle assembly transcript 1 (NEAT1) [1]

• Resistant Disease: Brain glioma [ICD-11: 2A00.0]
• Molecule Alteration: Down-regulation; Interaction
• Experimental Note: Discovered Using In-vivo Testing Model
• In Vitro Model: C6 cells; Brain; Rattus norvegicus (Rat); CVCL_0194
• Experiment for Molecule Alteration: qRT-PCR; Western bloting analysis; Immunofluorescence assay; ELISA assay; Luciferase assay; Overexpression assay
• Mechanism Description: LncRNA NEAT1 overexpression reversed ISL-mediated increase in miR-194-5p expression, and thereby attenuated FGF-2, TGF-beta and VEGF production.

Oral squamous cell carcinoma [ICD-11: 2B6E]

Drug Sensitivity Data Categorized by Their Corresponding Mechanisms

Unusual Activation of Pro-survival Pathway (UAPP)

Key Molecule: Threonine 34 phosphorylation (Thr34) [2]

• Sensitive Disease: Oral squamous cell carcinoma [ICD-11: 2B6E.0]
• Molecule Alteration: Phosphorylation; Down-regulation
• Experimental Note: Revealed Based on the Cell Line Data
• Cell Pathway Regulation: Akt-Wee1-CDK1 signaling pathway; Regulation; N.A.
• In Vitro Model: CAL-27 cells; Tongue; Homo sapiens (Human); CVCL_1107
• In Vitro Model: SCC25 cells; Oral; Homo sapiens (Human); CVCL_1682
• In Vitro Model: SCC-4 cells; Tongue; Homo sapiens (Human); CVCL_1684
• In Vitro Model: CCD-118Sk cells; N.A.; Homo sapiens (Human); CVCL_Y116
• In Vivo Model: Athymic female nude mice; Mus musculus
• Experiment for Molecule Alteration: Immunoblotting assay; Ubiquitination assay; Akt kinase activity assay; Immunohistochemistry
• Experiment for Drug Resistance: MTS assay; Soft agar assay; Plate colony formation assay; In vivo tumor growth assay; Blood assay
• Mechanism Description: Here, we found that ISL inhibited the viability and colony formation of OSCC, and promoted their apoptosis. The immunoblotting data showed that ISL treatment significantly decreased survivin expression. Mechanistically, ISL suppressed survivin phosphorylation on Thr34 by deregulating Akt-Wee1-CDK1 signaling, which facilitated survivin for ubiquitination degradation. ISL inhibited CAL27 tumor growth and decreased p-Akt and survivin expression in vivo. Meanwhile, survivin overexpression caused cisplatin resistance of OSCC cells. ISL alone or combined with cisplatin overcame chemoresistance in OSCC cells. Overall, our results revealed that ISL exerted potent inhibitory effects via inducing Akt-dependent survivin ubiquitination in OSCC cells.

References

• Ref 1: Inhibition of COX-2, mPGES-1 and CYP4A by isoliquiritigenin blocks the angiogenic Akt signaling in glioma through ceRNA effect of miR-194-5p and lncRNA NEAT1J Exp Clin Cancer Res. 2019 Aug 22;38(1):371. doi: 10.1186/s13046-019-1361-2.
• Ref 2: Isoliquiritigenin Inhibits Oral Squamous Cell Carcinoma and Overcomes Chemoresistance by Destruction of Survivin. Am J Chin Med. 2023;51(8):2221-2241.