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{{Short description|Antibiotic}} |
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{{Drugbox |
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{{Use mdy dates|date=March 2024}} |
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| verifiedrevid = 414579447 |
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{{cs1 config |name-list-style=vanc |display-authors=6}} |
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| IUPAC_name = 3-(((6-Deoxy-4-''O''-(3,5-dichloro-2-ethyl-4,6-dihydroxybenzoyl)-2-''O''-methyl-b-D-mannopyranosyl)oxy)-methyl)-12(''R'')--11(''S'')-ethyl-8(''S'')-hydroxy-18(''S'')-(1(''R'')-hydroxyethyl)-9,13,15-trimethyloxacyclooctadeca-3,5,9,13,15-pentaene-2-one |
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{{Infobox drug |
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| image = Lipiarmycin.png |
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| Verifiedfields = changed |
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| Watchedfields = changed |
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| verifiedrevid = 416459611 |
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| image = Fidaxomicin.svg |
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| width = |
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| alt = |
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| alt = |
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| CAS_number = 873857-62-6 |
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| caption = |
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| ATCvet = |
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<!-- Clinical data --> |
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| ATC_prefix = <!-- 'none' if uncategorised --> |
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| ATC_suffix = |
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| pronounce = |
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| tradename = Dificid, Dificlir |
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| PubChem = 11528171 |
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| Drugs.com = {{drugs.com|monograph|fidaxomicin}} |
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| DrugBank = |
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| MedlinePlus = |
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| DailyMedID = Fidaxomicin |
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| pregnancy_AU = B1 |
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| pregnancy_AU_comment = |
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| pregnancy_category = |
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| routes_of_administration = ] |
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| class = |
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| ATC_prefix = A07 |
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| ATC_suffix = AA12 |
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| ATC_supplemental = |
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<!-- Legal status --> |
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| legal_AU = S4 |
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| legal_AU_comment = |
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| legal_BR = <!-- OTC, A1, A2, A3, B1, B2, C1, C2, C3, C4, C5, D1, D2, E, F--> |
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| legal_BR_comment = |
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| legal_CA = Rx-only |
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| legal_CA_comment = |
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| legal_DE = <!-- Anlage I, II, III or Unscheduled--> |
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| legal_DE_comment = |
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| legal_NZ = <!-- Class A, B, C --> |
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| legal_NZ_comment = |
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| legal_UK = POM |
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| legal_UK_comment = |
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| legal_US = Rx-only |
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| legal_US_comment = |
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| legal_EU = Rx-only |
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| legal_EU_comment = <ref>{{cite web | title=Dificlir EPAR | website=] (EMA) | date=September 17, 2018 | url=https://www.ema.europa.eu/en/medicines/human/EPAR/dificlir | access-date=January 18, 2021}}</ref> |
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| legal_UN = <!-- N I, II, III, IV / P I, II, III, IV--> |
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| legal_UN_comment = |
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| legal_status = <!-- For countries not listed above --> |
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<!-- Pharmacokinetic data --> |
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| bioavailability = Minimal systemic absorption<ref name = TGA>{{cite web|title=Dificid|work=TGA eBusiness Services|publisher=Specialised Therapeutics Australia Pty Ltd|date=April 23, 2013|access-date=March 31, 2014|url=https://www.ebs.tga.gov.au/ebs/picmi/picmirepository.nsf/pdf?OpenAgent&id=CP-2013-PI-01580-1|format=PDF}}</ref> |
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| protein_bound = |
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| metabolism = |
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| metabolites = |
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| onset = |
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| elimination_half-life = 11.7 ± 4.80 hours<ref name = TGA/> |
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| duration_of_action = |
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| excretion = Urine (<1%), faeces (92%)<ref name = TGA/> |
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<!-- Identifiers --> |
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| CAS_number_Ref = {{cascite|correct|??}} |
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| CAS_number = 873857-62-6 |
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| CAS_supplemental = |
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| PubChem = 10034073 |
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| IUPHAR_ligand = |
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| DrugBank_Ref = {{drugbankcite|correct|drugbank}} |
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| DrugBank = DB08874 |
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| ChemSpiderID_Ref = {{chemspidercite|changed|chemspider}} |
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| ChemSpiderID = 8209640 |
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| UNII_Ref = {{fdacite|changed|FDA}} |
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| UNII = Z5N076G8YQ |
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| KEGG_Ref = {{keggcite|correct|kegg}} |
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| KEGG_Ref = {{keggcite|correct|kegg}} |
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| KEGG = D09394 |
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| KEGG = D09394 |
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| ChEBI_Ref = {{ebicite|changed|EBI}} |
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| C=52|H=74|Cl=2|O=18 |
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| ChEBI = 68590 |
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| bioavailability = |
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| ChEMBL_Ref = {{ebicite|changed|EBI}} |
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| protein_bound = |
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| ChEMBL = 1255800 |
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| metabolism = |
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| NIAID_ChemDB = |
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| elimination_half-life = |
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| excretion = Feces |
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| PDB_ligand = |
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| synonyms = Clostomicin B1, lipiarmicin, lipiarmycin, lipiarmycin A3, OPT-80, PAR 01, PAR-101, tiacumicin B |
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| pregnancy_AU = <!-- A / B1 / B2 / B3 / C / D / X --> |
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| pregnancy_US = <!-- A / B / C / D / X --> |
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<!-- Chemical and physical data --> |
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| pregnancy_category= |
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| IUPAC_name = 3-(((6-Deoxy-4-''O''-(3,5-dichloro-2-ethyl-4,6-dihydroxybenzoyl)-2-''O''-methyl-β-<small>D</small>-mannopyranosyl)oxy)-methyl)-12(''R'')--11(''S'')-ethyl-8(''S'')-hydroxy-18(''S'')-(1(''R'')-hydroxyethyl)-9,13,15-trimethyloxacyclooctadeca-3,5,9,13,15-pentaene-2-one |
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| legal_AU = <!-- S2, S3, S4, S5, S6, S7, S8, S9 or Unscheduled--> |
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| C=52 | H=74 | Cl=2 | O=18 |
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| legal_CA = <!-- Schedule I, II, III, IV, V, VI, VII, VIII --> |
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| SMILES = CC1/C=C(/(C/C=C/C=C(/C(=O)O(C/C=C(/C=C(/1O2(((C(O2)(C)C)OC(=O)C(C)C)O)O)\C)\C)(C)O)\CO3((((O3)C)OC(=O)C4=C(C(=C(C(=C4O)Cl)O)Cl)CC)O)OC)O)\C |
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| legal_UK = <!-- GSL, P, POM, CD, or Class A, B, C --> |
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| legal_US = Rx-only <!-- OTC / Rx-only / Schedule I, II, III, IV, V --> |
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| Jmol = |
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| StdInChI_Ref = {{stdinchicite|changed|chemspider}} |
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| legal_status = Phase III |
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| StdInChI = 1S/C52H74Cl2O18/c1-13-30-22-26(6)33(56)18-16-15-17-31(23-66-51-45(65-12)42(61)44(29(9)67-51)69-49(64)35-32(14-2)36(53)39(58)37(54)38(35)57)48(63)68-34(28(8)55)20-19-25(5)21-27(7)43(30)70-50-41(60)40(59)46(52(10,11)72-50)71-47(62)24(3)4/h15-17,19,21-22,24,28-30,33-34,40-46,50-51,55-61H,13-14,18,20,23H2,1-12H3/b16-15+,25-19+,26-22+,27-21+,31-17+/t28-,29-,30+,33+,34+,40-,41+,42+,43+,44-,45+,46+,50-,51-/m1/s1 |
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| routes_of_administration = Oral |
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| StdInChI_comment = |
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| StdInChIKey_Ref = {{stdinchicite|changed|chemspider}} |
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| StdInChIKey = ZVGNESXIJDCBKN-UUEYKCAUSA-N |
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| density = |
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| solubility = |
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}} |
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}} |
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'''Fidaxomicin''', sold under the brand name '''Dificid''' (by Merck) among others, is the first member of a class of narrow spectrum ] ] drugs called ]s.<ref>{{cite journal |doi=10.1358/dof.2006.031.06.1000709 |title=Tiacumicin B |year=2006 | vauthors = Revill P, Serradell N, Bolos J |journal=Drugs of the Future |volume=31 |issue=6 |pages=494}}</ref> It is a fermentation product obtained from the actinomycete '']'' subspecies ''hamdenesis''.<ref name=PrescribingInfo>{{cite web | title=Dificid- fidaxomicin tablet, film coated Dificid- fidaxomicin granule, for suspension | website=DailyMed | date=February 18, 2020 | url=https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=dd966338-c820-4270-b704-09ef75fa3ceb | access-date=March 26, 2020}}</ref><ref>{{cite journal | vauthors = | title = Fidaxomicin: Difimicin; Lipiarmycin; OPT 80; OPT-80; PAR 101; PAR-101 | journal = Drugs in R&D | volume = 10 | issue = 1 | pages = 37–45 | year = 2012 | pmid = 20509714 | pmc = 3585687 | doi = 10.2165/11537730-000000000-00000 }}</ref> |
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'''Fidaxomicin''' (also known as OPT-80 and PAR-101) is the first in a new class of narrow spectrum ] ] drugs.<ref>{{cite journal | author = Revill, P.; Serradell, N.; Bolos, J. | title = Tiacumicin B: macrolide antibiotic treatment of C. difficile-associated diarrhea | journal = Drugs of the Future | year = 2006 | volume = 31 | issue = 6 | pages = 494–497}}</ref> It is non-systemic, meaning it is minimally absorbed into the bloodstream, it is ], and it has demonstrated selective eradication of ] '']'' with minimal disruption to the multiple species of ] that make up the normal, healthy ]. The maintenance of normal physiological conditions in the colon can reduce the probability of '']'' infection recurrence.<ref> {{cite journal|title=OPT-80 Eliminates Clostridium difficile and Is Sparing of Bacteroides|journal=Antimicrobial Agents and Chemotherapy|date=2009-01|first=Thomas|last=Louie|coauthors=Judy Emery, Walter Krulicki, Brendan Byrne, and Manuel Mah|volume=535|issue=1|pages=261–263|pmid=18955523|format=|accessdate=2009-11-09|pmc=2612159|doi=10.1128/AAC.01443-07 }}</ref><ref> {{cite journal|doi=10.1016/j.jinf.2009.03.010|title=Recurrent Clostridium difficile infection: a review of risk factors, treatments, and outcomes|journal=Journal of Infection|date=2009-06|first=Stuart|last=Johnson|coauthors=|volume=58|issue=6|pages=403–410|pmid=19394704 |url=http://www.sciencedirect.com/science?_ob=PublicationURL&_tockey=%23TOC%236887%232009%23999419993%231131057%23FLA%23&_cdi=6887&_pubType=J&_auth=y&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=d064db6774b6e2dc79bf19d1bd1dc9d5|format=|accessdate=2009-11-10 }}</ref> |
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Fidaxomicin is minimally absorbed into the bloodstream when taken orally, is ], and selectively eradicates ] '']'' with relatively little disruption to the multiple species of ] that make up the normal, healthy ]. The maintenance of normal physiological conditions in the colon may reduce the probability of recurrence of ].<ref>{{cite journal | vauthors = Louie TJ, Emery J, Krulicki W, Byrne B, Mah M | title = OPT-80 eliminates Clostridium difficile and is sparing of bacteroides species during treatment of C. difficile infection | journal = Antimicrobial Agents and Chemotherapy | volume = 53 | issue = 1 | pages = 261–263 | date = January 2009 | pmid = 18955523 | pmc = 2612159 | doi = 10.1128/AAC.01443-07 }}</ref><ref>{{cite journal | vauthors = Johnson S | title = Recurrent Clostridium difficile infection: a review of risk factors, treatments, and outcomes | journal = The Journal of Infection | volume = 58 | issue = 6 | pages = 403–410 | date = June 2009 | pmid = 19394704 | doi = 10.1016/j.jinf.2009.03.010 }}</ref> |
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It is marketed by ], which acquired Cubist Pharmaceuticals in 2015, and had in turn bought the originating company, Optimer Pharmaceuticals. It is used for the treatment of ''Clostridioides difficile'' infection, which is also known as ''Clostridioides difficile''-associated diarrhea or ''Clostridioides difficile''-associated illness (CDI), and can develop into ''Clostridioides difficile'' colitis and pseudomembranous colitis. |
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It is being developed by Optimer Pharmaceuticals for treatment of '']'' infection. It is administered orally. |
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It is approved as a ].<ref>{{cite web | title=First-Time Generic Drug Approvals 2024 | website=U.S. ] (FDA) | date=March 8, 2024 | url=https://www.fda.gov/drugs/drug-and-biologic-approval-and-ind-activity-reports/first-generic-drug-approvals | access-date=March 9, 2024}}</ref> |
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It works by inhibiting the bacterial enzyme ], resulting in the death of '']''. It is active against ] bacteria especially ]. |
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==Mechanism== |
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Fidaxomicin binds to and prevents movement of the "switch regions" of bacterial RNA polymerase. Switch motion occurs during the opening and closing of the DNA:RNA clamp, a process that occurs throughout RNA transcription but is especially important in the opening of double-stranded DNA during the initiation of transcription.<ref>{{cite journal | vauthors = Srivastava A, Talaue M, Liu S, Degen D, Ebright RY, Sineva E, Chakraborty A, Druzhinin SY, Chatterjee S, Mukhopadhyay J, Ebright YW, Zozula A, Shen J, Sengupta S, Niedfeldt RR, Xin C, Kaneko T, Irschik H, Jansen R, Donadio S, Connell N, Ebright RH | title = New target for inhibition of bacterial RNA polymerase: 'switch region' | journal = Current Opinion in Microbiology | volume = 14 | issue = 5 | pages = 532–543 | date = October 2011 | pmid = 21862392 | pmc = 3196380 | doi = 10.1016/j.mib.2011.07.030 | author22-link = Richard H. Ebright }}</ref> It has minimal systemic absorption and a narrow spectrum of activity; it is active against ] bacteria, especially ]. The minimal inhibitory concentration (MIC) range for ''C. difficile'' (ATCC 700057) is 0.03–0.25 μg/mL.<ref name=PrescribingInfo/> |
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== Biosynthesis == |
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The biosynthetic pathway of fidaxomicin, also known as tiacumicin B, was first proposed in 2011 by Zhang et al. based on the identification of and sequence analysis of the tiacumicin B ''tia-''gene cluster. The biosynthesis begins with the formation of the core aglycone, tiacumicinone, done by a type I ] (PKS) coded for by the ''tiaA1-tiaA4'' genes. The PKS is composed of a loading domain and eight elongating domains. Tiacumicinone formation starts when the loading acyltransferase domain loads propionyl-CoA onto the loading acyl carrier protein (ACP) domain. The following eight modules extend and tailor the polyketide using malonyl-CoA, methylmalonyl-CoA, and ethylmalonyl-CoA. The final thioesterase domain hydrolyzes the polyketide to form the 18-membered tiacumicinone aglycone.<ref>{{cite journal | vauthors = Xiao Y, Li S, Niu S, Ma L, Zhang G, Zhang H, Zhang G, Ju J, Zhang C | title = Characterization of tiacumicin B biosynthetic gene cluster affording diversified tiacumicin analogues and revealing a tailoring dihalogenase | journal = Journal of the American Chemical Society | volume = 133 | issue = 4 | pages = 1092–1105 | date = February 2011 | pmid = 21186805 | doi = 10.1021/ja109445q }}</ref> Modification to the aglycone begins with oxidation at the C(20) position by TiaP2, a cytochrome P450. This is followed by attachment of ᴅ-noviose at the OH-C(11) position by the glycotransferase TiaG1. Next, the glycotransferase TiaG2 binds ᴅ-rhamnose at the OH-C(20) position followed by the attachment of an isobutyric ester at the OH-C(4’’) position of the noviose. TiaB, which codes for another type I PKS, forms an homoorsellinic acid moiety from propionyl-CoA and three malonyl-CoA elongating units that is coupled to rhamnose at the OH-C(4’) position by the TiaF, a ketoacyl ACP synthase. This is followed by chlorination of the aryl moiety by the halogenase TiaM and methylation of the OH-C(2’) position of rhamnose by the methyltransferase TiaS5. Lastly, there is another oxidation by the cytochrome P450 TiaP1 that oxidizes at the C(18) position of the aglycone to give tiacumicin B.<ref>{{cite journal | vauthors = Dorst A, Jung E, Gademann K | title = Recent Advances in Mode of Action and Biosynthesis Studies of the Clinically Used Antibiotic Fidaxomicin | journal = CHIMIA | volume = 74 | issue = 4 | pages = 270–273 | date = April 2020 | pmid = 32331545 | doi = 10.2533/chimia.2020.270 | s2cid = 216130499 | doi-access = free }}</ref> |
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==Clinical trials== |
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==Clinical trials== |
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Good results were reported in 2009 from a North American ] trial comparing it with oral ] for the treatment of '']'' Infection, or CDI<ref>, The Medical News, September 16, 2009</ref><ref>, Reuters, May 17, 2009</ref>The study met its primary endpoint of clinical cure, showing that fidaxomicin was non inferior to oral ] (92.1% vs. 89.8%). In addition, the study met its secondary endpoint of recurrence: 13.3% of the subjects had a recurrence with fidaxomicin vs. 24.0% with oral ], p=0.004. The study also met its exploratory endpoint of global cure (77.7% for fidaxomicin vs. 67.1% for vancomycin p=0.006.<ref> {{Cite document| first=Y. | last=Golan| coauthors=K.M. Mullane, M. Miller, K. Weiss, A. Lentnek, P. Sears, Y.K. Shue, S.L. Gorbach, T.J. Louie| contribution=Low Recurrence Rate Among Patients with C. difficile Infection Treated with Fidaxomicin| title=ICAAC 2009| editor-first=| editor-last=| coeditors=| publisher=Interscience Conference on Antimicrobial Agents and Chemotherapy| place=San Francisco, California| pages=| date=2009-09| year=2009| id= | contribution-url=http://www.icaac.org/| format=| accessdate=2009-11-09| postscript=<!-- Bot inserted parameter. Either remove it; or change its value to "." for the cite to end in a ".", as necessary. -->{{inconsistent citations}} }}</ref> ''Clinical cure'' was defined as patients requiring no further CDI therapy two days after completion of study medication. ''Global cure'' was defined as patients who were cured at the end of therapy and did not have a recurrence in the next 4 weeks.<ref> {{Cite document| first=S. | last=Gorbach| coauthors=K. Weiss, P. Sears, and J. Pullman| contribution=Safety of Fidaxomicin Versus Vancomycin in Treatment of Clostridium difficile Infection| title=ICAAC 2009| editor-first=| editor-last=| coeditors=| publisher=Interscience Conference on Antimicrobial Agents and Chemotherapy and American Society for Microbiology| place=San Francisco, California| pages=| date=2009-09| year=2009| id= | contribution-url=http://www.icaac.org/| format=| accessdate=2009-11-09| postscript=<!-- Bot inserted parameter. Either remove it; or change its value to "." for the cite to end in a ".", as necessary. -->{{inconsistent citations}} }}</ref> |
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Good results were reported by the company in 2009, from a North American ] comparing it with oral ] for the treatment of '']'' infection.<ref>{{cite press release |title=Optimer's North American phase 3 Fidaxomicin study results presented at the 49th ICAAC |publisher=Optimer Pharmaceuticals |date=September 16, 2009 |url=http://www.news-medical.net/news/20090916/Optimers-North-American-phase-3-Fidaxomicin-study-results-presented-at-the-49th-ICAAC.aspx |access-date=May 7, 2013}}</ref><ref>{{cite press release |title=Optimer Pharmaceuticals Presents Results From Fidaxomicin Phase 3 Study for the Treatment |publisher=Optimer Pharmaceuticals |date=May 17, 2009 |url=https://www.reuters.com/article/2009/05/17/idUS33839+17-May-2009+PRN20090517 |archive-url=https://web.archive.org/web/20121114115811/http://www.reuters.com/article/2009/05/17/idUS33839+17-May-2009+PRN20090517 |url-status=dead |archive-date=November 14, 2012 |access-date=May 7, 2013}}</ref> The study met its primary endpoint of clinical cure, showing that fidaxomicin was non-inferior to oral vancomycin (92.1% vs. 89.8%). In addition, the study met its secondary endpoint of recurrence: 13.3% of the subjects had a recurrence with fidaxomicin vs. 24.0% with oral vancomycin. The study also met its exploratory endpoint of global cure (77.7% for fidaxomicin vs. 67.1% for vancomycin).<ref>{{cite conference |vauthors=Golan Y, Mullane KM, Miller MA |title=Low recurrence rate among patients with ''C. difficile'' infection treated with fidaxomicin |conference=49th interscience conference on antimicrobial agents and chemotherapy |location=San Francisco |date=September 12–15, 2009}}</ref> ''Clinical cure'' was defined as patients requiring no further therapy for the treatment of ''C. difficile'' infection two days after completion of study medication. ''Global cure'' was defined as patients who were cured at the end of therapy and did not have a recurrence in the next four weeks.<ref>{{cite conference |vauthors=Gorbach S, Weiss K, Sears P, Pullman J |title=Safety of fidaxomicin versus vancomycin in treatment of ''Clostridium difficile'' infection |conference=49th interscience conference on antimicrobial agents and chemotherapy |location=San Francisco |date=September 12–15, 2009 }}</ref> |
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Fidaxomicin was shown to be as good as the standard-of-care, vancomycin, for treating ''Clostridioides difficile'' infection in a Phase III clinical trial published in February 2011.<ref>{{cite journal | vauthors = Louie TJ, Miller MA, Mullane KM, Weiss K, Lentnek A, Golan Y, Gorbach S, Sears P, Shue YK | title = Fidaxomicin versus vancomycin for Clostridium difficile infection | journal = The New England Journal of Medicine | volume = 364 | issue = 5 | pages = 422–431 | date = February 2011 | pmid = 21288078 | doi = 10.1056/NEJMoa0910812 | doi-access = free }}</ref> The authors also reported significantly fewer recurrences of infection, a frequent problem with ''C. difficile'', and similar drug side effects. |
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A second Phase 3 clinical trial of the same design is currently ongoing in North America and Europe.<ref></ref> Fidaxomicin has been granted fast track status by the ] (FDA). |
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Based on a multicenter clinical trial, fidaxomicin was reported well tolerated in children with ''Clostridioides difficile''–associated diarrhea and has a pharmacokinetic profile in children similar to that in adults.<ref>{{cite journal | vauthors = O'Gorman MA, Michaels MG, Kaplan SL, Otley A, Kociolek LK, Hoffenberg EJ, Kim KS, Nachman S, Pfefferkorn MD, Sentongo T, Sullivan JE, Sears P | title = Safety and Pharmacokinetic Study of Fidaxomicin in Children With Clostridium difficile-Associated Diarrhea: A Phase 2a Multicenter Clinical Trial | journal = Journal of the Pediatric Infectious Diseases Society | volume = 7 | issue = 3 | pages = 210–218 | date = August 2018 | pmid = 28575523 | doi = 10.1093/jpids/pix037 | doi-access = free }}</ref> |
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Sept 2010 : Good combined results from the two phase 3 trials.<ref>{{cite news |url=http://www.medpagetoday.com/MeetingCoverage/ICAAC/22198 |title= ICAAC: Novel Drug Trumps C. Diff Standard |date=15 Sep 2010 }}</ref> |
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<ref>{{cite news |url=http://www.drugs.com/clinical_trials/optimer-pharmaceuticals-announces-combined-data-fidaxomicin-phase-3-trials-clostridium-difficile-10446.html |title=Optimer Pharmaceuticals Announces Combined Data From Fidaxomicin Phase 3 Trials for the Treatment of Clostridium difficile Infection (CDI) Presented at IDSA |date=23 Oct 2010 }}</ref> |
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Regarding the high budget to spend for fidaxomicin, a systematic literature review published in 2017, showed that fidaxomicin was demonstrated to be cost-effective versus metronidazole and vancomycin in patients with ''Clostridioides difficile'' infection.<ref>{{cite journal | vauthors = Burton HE, Mitchell SA, Watt M | title = A Systematic Literature Review of Economic Evaluations of Antibiotic Treatments for Clostridium difficile Infection | journal = PharmacoEconomics | volume = 35 | issue = 11 | pages = 1123–1140 | date = November 2017 | pmid = 28875314 | pmc = 5656734 | doi = 10.1007/s40273-017-0540-2 }}</ref> |
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Target approval date is May 30, 2011. |
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==References== |
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{{reflist}} |
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==Approvals and indications== |
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On April 5, 2011, the drug won an FDA advisory panel's unanimous approval for the treatment of ''Clostridioides difficile'' infection,<ref>{{cite news |url=https://www.bloomberg.com/news/2011-04-05/optimer-wins-fda-advisory-panel-s-backing-for-fidaxomicin-1-.html |title=Optimer wins FDA panel's backing for antibiotic fidaxomicin |publisher=Bloomberg |date=April 5, 2011 | vauthors = Peterson M }}</ref> and gained full FDA approval on May 27, 2011.<ref>{{cite news |url=http://www.medicalnewstoday.com/articles/226796.php |title=Dificid (fidaxomicin) approved for Clostridium difficile-associated diarrhea |date=May 27, 2011 |work=Medical News Today | vauthors = Nordqvist C }}</ref> As of January 2020, fidaxomicin is FDA-approved for use in children aged 6 months and older for ''C. difficile'' associated diarrhea (CDAD).<ref name=":0">{{Cite web |date=January 2020 |title=Dificid (fidaxomicin) |url=https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/213138lbl.pdf |access-date=April 21, 2022 |website=U.S. ] (FDA) }}</ref> |
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== Adverse effects == |
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The most common side effects reported in adults with the use of fidaxomicin include nausea, abdominal pain, vomiting, anemia, ], and gastrointestinal hemorrhage.<ref name=":0"/> In children the most common side effects include fever, vomiting, diarrhea, constipation, abdominal pain, rash, and increased aminotransferases.<ref name=":0" /> |
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== References == |
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