Drug Information

Drug (ID: DG00985) and It's Reported Resistant Information

• Name: Fotemustine
• Synonyms: Fotemustine; 92118-27-9; Diethyl (1-(3-(2-chloroethyl)-3-nitrosoureido)ethyl)phosphonate; Muphoran; Mustophorane; Fotemustina; Servier-10036; S 10036; Mustoforan; UNII-UPB2NN83AR; UPB2NN83AR; S-10036; UNII-QY93P3GN94; QY93P3GN94; (+-)-Diethyl (1-(3-(2-chloroethyl)-3-nitrosoureido)ethyl)phosphonate; MFCD00866278; Fotemustinum [Latin]; Diethyl-1-(3-(2-chloroethyl)-3-nitrosoureido)ethylphosphonate; Fotemustina [Spanish]; Fotemustinum; C9H19ClN3O5P; SMR002529685; CCRIS 6337; Fotemustine [INN:BAN]; HSDB 7762; Muphoran (TN); Fotemustine, (+)-; Fotemustine, (-)-; 1-(2-chloroethyl)-3-(1-diethoxyphosphorylethyl)-1-nitrosourea; Fotemustine (INN/BAN); SCHEMBL8880; MLS006010211; MLS006010716; CHEMBL549386; 6-Amino-3-hydroxy(1h)indazole; Fotemustine, >=98% (HPLC); DTXSID80869091; CHEBI:131852; BCP07342; HY-B0733; AKOS015920275; DS-1395; P-[1-[[[(2-Chloroethyl)nitrosoamino]carbonyl]amino]ethyl]-phosphonic acid diethyl ester; Phosphonic acid, (1-((((2-chloroethyl)nitrosoamino)carbonyl)amino)ethyl)-, diethyl ester; NCGC00346829-01; NCGC00346829-03; K679; DB-057290; FT-0630979; D07255; 118F279; A844148; SR-01000944936; Q1439555; SR-01000944936-1; diethyl 1-(3-(2-chloroethyl)-3-nitrosoureido)ethylphosphonate; 1-(2-chloroethyl)-3-(1-diethoxyphosphorylethyl)-1-nitroso-urea; diethyl (1-{[(2-chloroethyl)(nitroso)carbamoyl]amino}ethyl)phosphonate; diethyl (1-{[N-(2-chloroethyl)-N'-oxohydrazinecarbonyl]amino}ethyl)phosphonate; 191219-77-9; 191220-84-5; Muphoran; ; ; Mustoforan; ; ; S-10036; ; ; 1-(2-Chloroethyl)-3-(1-diethoxyphosphorylethyl)-1-nitrosourea; Phosphonic acid, (1-((((2-chloroethyl)nitrosoamino)carbonyl)amino)ethyl)-, diethyl ester, (+)-; Phosphonic acid, (1-((((2-chloroethyl)nitrosoamino)carbonyl)amino)ethyl)-, diethyl ester, (-)-
• Indication:
  In total 1 Indication(s)
  Solid tumour/cancer [ICD-11: 2A00-2F9Z]; Approved; [1]
• Drug Resistance Disease(s):
  Disease(s) with Resistance Information Validated by in-vivo Model for This Drug (1 diseases)
  Endometriosis [ICD-11: GA10]; [1]
• Target: Cytoplasmic thioredoxin reductase (TXNRD1); TRXR1_HUMAN; [1]
• Formula: C9H19ClN3O5P
• IsoSMILES: CCOP(=O)(C(C)NC(=O)N(CCCl)N=O)OCC
• InChI: 1S/C9H19ClN3O5P/c1-4-17-19(16,18-5-2)8(3)11-9(14)13(12-15)7-6-10/h8H,4-7H2,1-3H3,(H,11,14)
• InChIKey: YAKWPXVTIGTRJH-UHFFFAOYSA-N
• PubChem CID: 104799
• ChEBI ID: CHEBI:131852
• TTD Drug ID: D0S1ZB
• DrugBank ID: DB04106

Type(s) of Resistant Mechanism of This Drug

  UAPP: Unusual Activation of Pro-survival Pathway

Drug Resistance Data Categorized by Their Corresponding Diseases

ICD-16: Genitourinary system diseases

Endometriosis [ICD-11: GA10]

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Unusual Activation of Pro-survival Pathway (UAPP)

Key Molecule: Prostaglandin G/H synthase 2 (PTGS2) [1]

• Molecule Alteration: Expression; Up-regulation
• Resistant Disease: Endometriosis [ICD-11: GA10.0]
• Experimental Note: Discovered Using In-vivo Testing Model
• Cell Pathway Regulation: MAPK signaling pathway; Activation; hsa04010
• In Vivo Model: Female Sprague-Dawley rats model; Rattus norvegicus
• Experiment for Molecule Alteration: Western blotting analysis
• Mechanism Description: Fotemustine and dexamethasone administration had anti-apoptotic activity, restoring the impaired mechanism (TUNEL assay and Western blot analysis of Bax and Bcl-2). Moreover, no gastric disfunction was detected (histological analysis of stomachs). Thus, our data showed that the combined therapy of fotemustine and dexamethasone reduced endometriosis-induced inflammation, hyperproliferation and apoptosis resistance.

Key Molecule: DNA-binding factor KBF1 (p105) (NFKB1) [1]

• Molecule Alteration: Expression; Up-regulation
• Resistant Disease: Endometriosis [ICD-11: GA10.0]
• Experimental Note: Discovered Using In-vivo Testing Model
• Cell Pathway Regulation: MAPK signaling pathway; Activation; hsa04010
• In Vivo Model: Female Sprague-Dawley rats model; Rattus norvegicus
• Experiment for Molecule Alteration: Western blotting analysis
• Mechanism Description: Fotemustine and dexamethasone administration had anti-apoptotic activity, restoring the impaired mechanism (TUNEL assay and Western blot analysis of Bax and Bcl-2). Moreover, no gastric disfunction was detected (histological analysis of stomachs). Thus, our data showed that the combined therapy of fotemustine and dexamethasone reduced endometriosis-induced inflammation, hyperproliferation and apoptosis resistance.

Key Molecule: Prostaglandin E2 receptor EP3 subtype (PE2R3) [1]

• Molecule Alteration: Expression; Up-regulation
• Resistant Disease: Endometriosis [ICD-11: GA10.0]
• Experimental Note: Discovered Using In-vivo Testing Model
• Cell Pathway Regulation: MAPK signaling pathway; Activation; hsa04010
• In Vivo Model: Female Sprague-Dawley rats model; Rattus norvegicus
• Experiment for Molecule Alteration: Western blotting analysis
• Mechanism Description: Fotemustine and dexamethasone administration had anti-apoptotic activity, restoring the impaired mechanism (TUNEL assay and Western blot analysis of Bax and Bcl-2). Moreover, no gastric disfunction was detected (histological analysis of stomachs). Thus, our data showed that the combined therapy of fotemustine and dexamethasone reduced endometriosis-induced inflammation, hyperproliferation and apoptosis resistance.

References

• Ref 1: Regulation of Inflammatory and Proliferative Pathways by Fotemustine and Dexamethasone in Endometriosis .Int J Mol Sci. 2021 Jun 1;22(11):5998. doi: 10.3390/ijms22115998. 10.3390/ijms22115998