Page last updated: 2024-11-08

efinaconazole

Description Research Excerpts Clinical Trials Roles Classes Pathways Study Profile Bioassays Related Drugs Related Conditions Protein Interactions Research Growth Market Indicators

Description

efinaconazole: an antifungal agent; structure in first source [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

efinaconazole : A member of the class of triazoles that is butan-2-ol which is substituted at positions 1, 2, and 3 by 1,2,4-triazol-1-yl, 2,4-difluorophenyl, and 4-methylenepiperidin-1-yl groups, respectively (the 2R,3R stereoisomer). It is an antifungal drug used for the topical treatment of onychomycosis (a nail infection caused mainly by dermatophytes). [Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Cross-References

ID SourceID
PubMed CID489181
CHEMBL ID2103877
CHEBI ID82718
SCHEMBL ID300738
MeSH IDM0584821

Synonyms (69)

Synonym
(2r, 3r)-2-(2,4-difluorophenyl)-3-(4-methylenepiperidyl)-1-(1,2,4-triazolyl)butan-2-ol
efinaconazole
(2r,3r)-2-(2,4-difluorophenyl)-3-(4-methylene-1-piperidyl)-1-(1,2,4-triazol-1-yl)butan-2-ol
kp103
kp-103
kp 103
(2r,3r)-2-(2,4-difluorophenyl)-3-(4-methylidenepiperidin-1-yl)-1-(1,2,4-triazol-1-yl)butan-2-ol
efinaconazole (jan/usan/inn)
D10021
164650-44-6
clenafin (tn)
jublia (tn)
(2r,3r)-2-(2,4-difluorofenil)-3-(4-metilenopiperidin-1-il)-1-(1h-1,2,4-triazin-1-il)butan-2-ol
unii-j82sb7fxwb
jublia
efinaconazole [usan:inn]
1-piperidineethanol, alpha-(2,4-difluorophenyl)-beta-methyl-4-methylene-alpha-(1h-1,2,4-triazol-1- ylmethyl)-, (alphar,betar)-
hsdb 8341
j82sb7fxwb ,
(2r,3r)-2-(2,4-difluorophenyl)-3-(4-methylidenepiperidin-1-yl)-1-(1h-1,2,4-triazol-1-yl)butan-2-ol
clenafin
CHEMBL2103877
chebi:82718 ,
idp-108
S5025
SCHEMBL300738
efinaconazole [orange book]
efinaconazole [usan]
1-piperidineethanol, .alpha.-(2,4-difluorophenyl)-.beta.-methyl-4-methylene-.alpha.-(1h-1,2,4-triazol-1-ylmethyl)-,(.alpha.r,.beta.r)-
efinaconazole [jan]
efinaconazole [mi]
1-piperidineethanol, .alpha.-(2,4-difluorophenyl)-.beta.-methyl-4-methylene-.alpha.-(1h-1,2,4-triazol-1-ylmethyl)-, (r-(r*,r*))-
(2r,3r)-2-(2,4-difluorophenyl)-3-(4-methylenepiperidin-1-yl)-1-(1h-1,2,4-triazol-1-yl)butan-2-ol
efinaconazole [inn]
efinaconazole [who-dd]
efinaconazole [vandf]
efinaconazolum
efinaconazol
CS-3500
(2r,3r)-2-(2,4-difluorophenyl)-3-(4-methylenepiperidine-1-yl)-1-(1h-1,2,4-triazole-1-yl)butane-2-ol
(2r,3r)-2-(2,4-difluorophenyl)-3-(4-methylenepiperidino)-1-(1h-1,2,4-triazol-1-yl)butan-2-ol
NFEZZTICAUWDHU-RDTXWAMCSA-N
c18h22f2n4o
AC-30630
HY-15660
DTXSID40167787 ,
DB09040
(2r,3r)-2-(2,4-difluorophenyl)-3-(4-methylene-1-piperidinyl)-1-(1h-1,2,4-triazol-1-yl)-2-butanol
AKOS027323571
mfcd00936406
NCGC00390702-01
efinaconazole(kp-103)
EX-A2643
efinaconazole; kp-103
Q21011225
AS-30126
164905-19-5
BCP11665
1-piperidineethanol, alpha-(2,4-difluorophenyl)-beta-methyl-4-methylene-alpha-(1h-1,2,4-triazol-1-ylmethyl)-, (alphar,betar)-
NCGC00390702-03
CCG-268012
NCGC00390702-02
A854585
(alphar,betar)-alpha-(2,4-difluorophenyl)-beta-methyl-4-methylene-alpha-(1h-1,2,4-triazol-1-ylmethyl)-1-piperidineethanol
1-piperidineethanol, alpha-(2,4-difluorophenyl)-beta-methyl-4-methylene-alpha-(1h-1,2,4-triazol-1-ylmethyl)-,(alphar,betar)-
dtxcid3090278
d01ac19
1-piperidineethanol, alpha-(2,4-difluorophenyl)-beta-methyl-4-methylene-alpha-(1h-1,2,4-triazol-1-ylmethyl)-, (r-(r*,r*))-
EN300-7393023

Research Excerpts

Overview

Efinaconazole is a novel triazole antifungal drug for the topical treatment of onychomycosis, a nail infection caused mainly by dermatophytes. It is a CYP inhibitor and its lowest ki is 91 ng/mL for CYP2C9.

ExcerptReferenceRelevance
"Efinaconazole 10% solution is a triazole antifungal drug developed in Japan."( Characteristics and Efficacy of Two Topical Therapeutic Agents for Onychomycosis.
Kawai, M, 2019
)
1.24
"Efinaconazole is a topical antifungal drug approved in Japan for tinea unguium. "( Topical efinaconazole: A sequential combination therapy with oral terbinafine for refractory tinea unguium.
Aoi, J; Fukushima, S; Kashiwada-Nakamura, K; Kubo, M; Makino, K; Noguchi, H, 2021
)
2.5
"Efinaconazole 10% solution is an azole antifungal indicated for topical treatment of toenail onychomycosis in pediatric and adult patients. "( Efinaconazole topical solution (10%) for the treatment of onychomycosis in adult and pediatric patients.
Gupta, AK; Vlahovic, TC, 2022
)
3.61
"Efinaconazole is a novel antifungal agent, which has proven to be particularly effective against onychomycosis compared with conventional antifungal agents."( Evaluation of drug susceptibility test for Efinaconazole compared with conventional antifungal agents.
Hur, MS; Jung, WH; Lee, YW; Park, M, 2019
)
1.5
"Efinaconazole is a CYP inhibitor like other azole antifungals, and its lowest ki is 91 ng/mL for CYP2C9, a >130-fold higher concentration than the mean steady state Cmax observed in patients."( Safety and pharmacokinetics of efinaconazole 10% solution in healthy volunteers and patients with severe onychomycosis.
Jarratt, M; Kodera, N; Pillai, R; Siu, WJ; Smith, K; Yamakawa, E, 2013
)
1.4
"Efinaconazole solution 10% is a new triazole antifungal agent specifically developed for the treatment of onychomycosis."( Efinaconazole solution 10%: topical antifungal therapy for toenail onychomycosis.
Tosti, A, 2013
)
2.55
"Efinaconazole is an emerging antifungal therapy for the topical treatment of onychomycosis. "( Efinaconazole: a new topical treatment for onychomycosis.
Gupta, AK; Simpson, FC,
)
3.02
"Efinaconazole is a novel triazole antifungal drug for the topical treatment of onychomycosis, a nail infection caused mainly by dermatophytes. "( In vitro and in vivo assessment of dermatophyte acquired resistance to efinaconazole, a novel triazole antifungal.
Iwata, A; Katafuchi-Nagashima, M; Kumagai, N; Pillai, R; Sugiura, K; Tatsumi, Y; Watanabe, Y, 2014
)
2.08
"Efinaconazole is a triazole developed as a 10% solution for topical treatment of onychomycosis, a common fungal nail infection. "( Nonclinical safety assessment of Efinaconazole Solution (10%) for onychomycosis treatment.
Calvarese, B; Glynn, M; Jo, W; Minowa, K; Mutter, L; Nejishima, H; Pillai, R; Sanada, H; Senda, H, 2014
)
2.13
"Efinaconazole 10% solution is a new triazole antifungal agent developed for the topical treatment of onychomycosis. "( Efinaconazole 10% solution in the treatment of onychomycosis of the toenails.
Joseph, WS; Olin, JT; Pillai, R; Vlahovic, TC,
)
3.02
"Efinaconazole is a new triazole antifungal for topical treatment of onychomycosis. "( Efinaconazole: Developmental and reproductive toxicity potential of a novel antifungal azole.
Glynn, M; Jo, W; Matsuuchi, H; Minowa, K; Mutter, L; Nejishima, H; Okamura, H; Pillai, R; Sanada, H, 2015
)
3.3
"Efinaconazole 10 % solution is a new triazole antifungal agent developed for the topical treatment of fungal infections of the nails. "( Effect of intratympanic application of efinaconazole 10 % solution in the guinea pig.
Arakawa, K; Hidaka, H; Honkura, Y; Ikeda, R; Katori, Y; Kawase, T; Nomura, K; Oshima, H, 2016
)
2.15
"Efinaconazole 10% solution is a new topical antifungal recently approved and sold in Canada, the United States and Japan for the treatment of mild-to-moderate toenail onychomycosis."( How effective is efinaconazole in the management of onychomycosis?
Cernea, M; Gupta, AK, 2016
)
1.5
"Efinaconazole is a safe and effective treatment for onychomycosis that can be used in a wide range of patients due to its broad-spectrum antifungal activity and low rate of treatment-related adverse events. "( How effective is efinaconazole in the management of onychomycosis?
Cernea, M; Gupta, AK, 2016
)
2.22

Effects

Efinaconazole has shown a broad spectrum of antifungal activity in vitro and is more potent than ciclopirox against common onychomycosis pathogens. It has low ungual penetration due to its low keratin binding properties.

ExcerptReferenceRelevance
"Efinaconazole has a broad spectrum of antifungal activity in vitro and is more potent than ciclopirox against common onychomycosis pathogens. "( Efinaconazole topical solution, 10%: the development of a new topical treatment for toenail onychomycosis.
Pollak, RA, 2014
)
3.29
"Efinaconazole 10% has been shown to be safe and efficacious regardless of disease severity/duration at baseline; patient gender, ethnicity, or age (including pediatrics); or comorbidities such as diabetes or tinea pedis."( Efinaconazole topical solution (10%) for the treatment of onychomycosis in adult and pediatric patients.
Gupta, AK; Vlahovic, TC, 2022
)
2.89
"Efinaconazole has shown a broad spectrum of antifungal activity in vitro and is more potent than ciclopirox against common onychomycosis pathogens."( Efinaconazole solution 10%: topical antifungal therapy for toenail onychomycosis.
Tosti, A, 2013
)
2.55
"Efinaconazole has lower minimum inhibitory concentrations than terbinafine, ciclopirox, itraconazole and amorolfine in Trichophyton rubrum, Trichophyton mentagrophytes and Candida albicans."( Efinaconazole (Jublia) for the treatment of onychomycosis.
Gupta, AK; Simpson, FC, 2014
)
2.57
"Efinaconazole has a broad spectrum of antifungal activity in vitro and is more potent than ciclopirox against common onychomycosis pathogens. "( Efinaconazole topical solution, 10%: the development of a new topical treatment for toenail onychomycosis.
Pollak, RA, 2014
)
3.29
"Efinaconazole has broad-spectrum antifungal activity against dermatophytes, nondermatophyte molds and yeasts, and high ungual penetration due to its low keratin binding properties."( How effective is efinaconazole in the management of onychomycosis?
Cernea, M; Gupta, AK, 2016
)
1.5

Actions

ExcerptReferenceRelevance
"Efinaconazole has lower minimum inhibitory concentrations than terbinafine, ciclopirox, itraconazole and amorolfine in Trichophyton rubrum, Trichophyton mentagrophytes and Candida albicans."( Efinaconazole (Jublia) for the treatment of onychomycosis.
Gupta, AK; Simpson, FC, 2014
)
2.57

Treatment

Efinaconazole topical solution, 10%, was significantly more effective than vehicle use irrespective of the coexistence of tinea pedis or its treatment.

ExcerptReferenceRelevance
"Efinaconazole-treated polished nails showed substantial polish changes after the first day of treatment, with polish appearance and discoloration progressively worsening over 7 days of treatment."( Evaluation of the Appearance of Nail Polish Following Daily Treatment of Ex Vivo Human Fingernails With Topical Solutions of Tavaborole or Efinaconazole.
Chanda, S; Coronado, D; Merchant, T; Vlahovic, TC; Zane, LT, 2016
)
1.36
"Treatment with efinaconazole topical solution, 10%, was significantly more effective than vehicle use irrespective of the coexistence of tinea pedis or its treatment. "( Efinaconazole Topical Solution, 10% Efficacy in Patients with Onychomycosis and Coexisting Tinea Pedis.
Caldwell, B; Markinson, B, 2015
)
2.21

Toxicity

Efinaconazole was safe and efficacious in pediatric participants with mild-to-severe onychomycosis, with improved mycologic cure and complete cure rates compared with adults. Rat embryo-fetal and perinatal pup lethality was the most sensitive (NOAEL=5mg/kg/day) efinaconzole developmental toxicity and was noted at maternally toxic doses.

ExcerptReferenceRelevance
" Efinaconazole was well tolerated in both studies; no drug-related adverse events were reported."( Safety and pharmacokinetics of efinaconazole 10% solution in healthy volunteers and patients with severe onychomycosis.
Jarratt, M; Kodera, N; Pillai, R; Siu, WJ; Smith, K; Yamakawa, E, 2013
)
1.59
" Treatment associated adverse events in the efinaconazole 10% solution group were similar to vehicle and limited to local site reactions (2%)."( The efficacy and safety of efinaconazole 10% solution for treatment of mild to moderate onychomycosis: a pooled analysis of two phase 3 randomized trials.
Elewski, BE; Gupta, AK; Ieda, C; Kang, R; Kawabata, H; Olin, JT; Pillai, R; Sugarman, JL; Watanabe, S, 2014
)
0.96
" Rat embryo-fetal and perinatal pup lethality was the most sensitive (NOAEL=5mg/kg/day) efinaconazole developmental toxicity and was noted at maternally toxic doses."( Efinaconazole: Developmental and reproductive toxicity potential of a novel antifungal azole.
Glynn, M; Jo, W; Matsuuchi, H; Minowa, K; Mutter, L; Nejishima, H; Okamura, H; Pillai, R; Sanada, H, 2015
)
2.08
" There are limited data on adverse events associated with the newer topical onychomycosis drugs."( Retrospective analysis of adverse events with topical onychomycosis medications reported to the United States Food and Drug Administration.
Lipner, SR; Wang, Y, 2020
)
0.56
" The medication was well tolerated, with 4 local adverse events and no significant adverse events."( Efficacy and Safety of Efinaconazole 10% Solution in the Treatment of Onychomycosis in Diabetic Patients.
Hamedani, E; Harkless, L; Navarrete, R; Seun, J; Shofler, D; Thamby, R, 2020
)
0.87
"Efinaconazole was safe and efficacious in pediatric participants with mild-to-severe onychomycosis, with improved mycologic cure and complete cure rates compared with adults from two 52-week studies."( Safety, Pharmacokinetics, and Efficacy of Efinaconazole 10% Topical Solution for Onychomycosis Treatment in Pediatric Patients.
Eichenfield, LF; Elewski, B; Guenin, E; Gupta, AK; Pillai, R; Rosen, T; Stein Gold, L; Sugarman, JL; Vlahovic, TC, 2020
)
2.27
" Mild to moderate application site reactions were the only efinaconazole-related adverse events in 8 patients (7."( Long-term Efficacy and Safety of Once-daily Efinaconazole 10% Topical Solution (Jublia) for Dermatophyte Toenail Onychomycosis: An Interim Analysis.
Cooper, EA; Gupta, AK, 2021
)
1.13

Pharmacokinetics

ExcerptReferenceRelevance
" Efinaconazole is a CYP inhibitor like other azole antifungals, and its lowest ki is 91 ng/mL for CYP2C9, a >130-fold higher concentration than the mean steady state Cmax observed in patients."( Safety and pharmacokinetics of efinaconazole 10% solution in healthy volunteers and patients with severe onychomycosis.
Jarratt, M; Kodera, N; Pillai, R; Siu, WJ; Smith, K; Yamakawa, E, 2013
)
1.59

Bioavailability

ExcerptReferenceRelevance
" KP-103 proved to be highly effective in achieving mycological cure and preventing relapse against tinea pedis presumably because of its good bioavailability in the skin based on its low keratin-affinity, along with its potent antifungal activity."( In vivo fungicidal effect of KP-103 in a guinea pig model of interdigital tinea pedis determined by using a new method for removing the antimycotic carryover effect.
Arika, T; Tatsumi, Y; Yamaguchi, H; Yokoo, M, 2002
)
0.31
"The ATP-binding cassette transporter P-glycoprotein (P-gp) is known to limit both brain penetration and oral bioavailability of many chemotherapy drugs."( A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
Ambudkar, SV; Brimacombe, KR; Chen, L; Gottesman, MM; Guha, R; Hall, MD; Klumpp-Thomas, C; Lee, OW; Lee, TD; Lusvarghi, S; Robey, RW; Shen, M; Tebase, BG, 2019
)
0.51

Dosage Studied

The concentration-time profiles for efinaconazole and its major metabolite were relatively stable, with only minor fluctuations during the 24-hour dosing interval. Nail polish appearance after application of tavaborole (dropper) or efin Baconazole (brush) was evaluated.

ExcerptRelevanceReference
" Nail polish appearance after application of tavaborole (dropper) or efinaconazole (brush); respective applicator appearance; presence of color transfer from respective applicators; and color transfer to remaining solutions after dosing of polished nails were evaluated."( Evaluation of the Appearance of Nail Polish Following Daily Treatment of Ex Vivo Human Fingernails With Topical Solutions of Tavaborole or Efinaconazole.
Chanda, S; Coronado, D; Merchant, T; Vlahovic, TC; Zane, LT, 2016
)
0.87
" Dropper and brush applicators were applied to white watercolor paper immediately after dosing to evaluate color transfer from polished nails."( Evaluation of the Appearance of Nail Polish Following Daily Treatment of Ex Vivo Human Fingernails With Topical Solutions of Tavaborole or Efinaconazole.
Chanda, S; Coronado, D; Merchant, T; Vlahovic, TC; Zane, LT, 2016
)
0.64
" The concentration-time profiles for efinaconazole and its major metabolite were relatively stable, with only minor fluctuations during the 24-hour dosing interval."( Safety, Pharmacokinetics, and Efficacy of Efinaconazole 10% Topical Solution for Onychomycosis Treatment in Pediatric Patients.
Eichenfield, LF; Elewski, B; Guenin, E; Gupta, AK; Pillai, R; Rosen, T; Stein Gold, L; Sugarman, JL; Vlahovic, TC, 2020
)
1.1
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (1)

RoleDescription
EC 1.14.13.70 (sterol 14alpha-demethylase) inhibitorAn EC 1.14.13.* (oxidoreductase acting on paired donors, incorporating 1 atom of oxygen, with NADH or NADPH as one donor) inhibitor that interferes with the action of EC 1.14.13.70 (sterol 14alpha-demethylase).
[role information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Drug Classes (7)

ClassDescription
organofluorine compoundAn organofluorine compound is a compound containing at least one carbon-fluorine bond.
olefinic compoundAny organic molecular entity that contains at least one C=C bond.
piperidines
tertiary alcoholA tertiary alcohol is a compound in which a hydroxy group, -OH, is attached to a saturated carbon atom which has three other carbon atoms attached to it.
tertiary amino compoundA compound formally derived from ammonia by replacing three hydrogen atoms by organyl groups.
conazole antifungal drugAny conazole antifungal agent that has been used for the treatment of fungal infections in animals or humans.
triazole antifungal drugAny triazole antifungal agent that has been used for the treatment of fungal infections in humans or animals.
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Protein Targets (7)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
cytochrome P450 family 3 subfamily A polypeptide 4Homo sapiens (human)Potency1.34500.01237.983543.2770AID1645841
GVesicular stomatitis virusPotency0.47720.01238.964839.8107AID1645842
cytochrome P450 2D6Homo sapiens (human)Potency23.91850.00108.379861.1304AID1645840
Interferon betaHomo sapiens (human)Potency0.47720.00339.158239.8107AID1645842
HLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)Potency0.47720.01238.964839.8107AID1645842
Inositol hexakisphosphate kinase 1Homo sapiens (human)Potency0.47720.01238.964839.8107AID1645842
cytochrome P450 2C9, partialHomo sapiens (human)Potency0.47720.01238.964839.8107AID1645842
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (45)

Processvia Protein(s)Taxonomy
cell surface receptor signaling pathway via JAK-STATInterferon betaHomo sapiens (human)
response to exogenous dsRNAInterferon betaHomo sapiens (human)
B cell activation involved in immune responseInterferon betaHomo sapiens (human)
cell surface receptor signaling pathwayInterferon betaHomo sapiens (human)
cell surface receptor signaling pathway via JAK-STATInterferon betaHomo sapiens (human)
response to virusInterferon betaHomo sapiens (human)
positive regulation of autophagyInterferon betaHomo sapiens (human)
cytokine-mediated signaling pathwayInterferon betaHomo sapiens (human)
natural killer cell activationInterferon betaHomo sapiens (human)
positive regulation of peptidyl-serine phosphorylation of STAT proteinInterferon betaHomo sapiens (human)
cellular response to interferon-betaInterferon betaHomo sapiens (human)
B cell proliferationInterferon betaHomo sapiens (human)
negative regulation of viral genome replicationInterferon betaHomo sapiens (human)
innate immune responseInterferon betaHomo sapiens (human)
positive regulation of innate immune responseInterferon betaHomo sapiens (human)
regulation of MHC class I biosynthetic processInterferon betaHomo sapiens (human)
negative regulation of T cell differentiationInterferon betaHomo sapiens (human)
positive regulation of transcription by RNA polymerase IIInterferon betaHomo sapiens (human)
defense response to virusInterferon betaHomo sapiens (human)
type I interferon-mediated signaling pathwayInterferon betaHomo sapiens (human)
neuron cellular homeostasisInterferon betaHomo sapiens (human)
cellular response to exogenous dsRNAInterferon betaHomo sapiens (human)
cellular response to virusInterferon betaHomo sapiens (human)
negative regulation of Lewy body formationInterferon betaHomo sapiens (human)
negative regulation of T-helper 2 cell cytokine productionInterferon betaHomo sapiens (human)
positive regulation of apoptotic signaling pathwayInterferon betaHomo sapiens (human)
response to exogenous dsRNAInterferon betaHomo sapiens (human)
B cell differentiationInterferon betaHomo sapiens (human)
natural killer cell activation involved in immune responseInterferon betaHomo sapiens (human)
adaptive immune responseInterferon betaHomo sapiens (human)
T cell activation involved in immune responseInterferon betaHomo sapiens (human)
humoral immune responseInterferon betaHomo sapiens (human)
positive regulation of T cell mediated cytotoxicityHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
adaptive immune responseHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
antigen processing and presentation of endogenous peptide antigen via MHC class I via ER pathway, TAP-independentHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
regulation of T cell anergyHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
defense responseHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
immune responseHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
detection of bacteriumHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
regulation of interleukin-12 productionHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
regulation of interleukin-6 productionHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
protection from natural killer cell mediated cytotoxicityHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
innate immune responseHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
regulation of dendritic cell differentiationHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
antigen processing and presentation of endogenous peptide antigen via MHC class IbHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
inositol phosphate metabolic processInositol hexakisphosphate kinase 1Homo sapiens (human)
phosphatidylinositol phosphate biosynthetic processInositol hexakisphosphate kinase 1Homo sapiens (human)
negative regulation of cold-induced thermogenesisInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol phosphate biosynthetic processInositol hexakisphosphate kinase 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (18)

Processvia Protein(s)Taxonomy
cytokine activityInterferon betaHomo sapiens (human)
cytokine receptor bindingInterferon betaHomo sapiens (human)
type I interferon receptor bindingInterferon betaHomo sapiens (human)
protein bindingInterferon betaHomo sapiens (human)
chloramphenicol O-acetyltransferase activityInterferon betaHomo sapiens (human)
TAP bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
signaling receptor bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
protein bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
peptide antigen bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
TAP bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
protein-folding chaperone bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
inositol-1,3,4,5,6-pentakisphosphate kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol hexakisphosphate kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol heptakisphosphate kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol hexakisphosphate 5-kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
protein bindingInositol hexakisphosphate kinase 1Homo sapiens (human)
ATP bindingInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol hexakisphosphate 1-kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol hexakisphosphate 3-kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol 5-diphosphate pentakisphosphate 5-kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol diphosphate tetrakisphosphate kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (22)

Processvia Protein(s)Taxonomy
extracellular spaceInterferon betaHomo sapiens (human)
extracellular regionInterferon betaHomo sapiens (human)
Golgi membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
endoplasmic reticulumHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
Golgi apparatusHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
plasma membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
cell surfaceHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
ER to Golgi transport vesicle membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
secretory granule membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
phagocytic vesicle membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
early endosome membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
recycling endosome membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
extracellular exosomeHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
lumenal side of endoplasmic reticulum membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
MHC class I protein complexHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
extracellular spaceHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
external side of plasma membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
fibrillar centerInositol hexakisphosphate kinase 1Homo sapiens (human)
nucleoplasmInositol hexakisphosphate kinase 1Homo sapiens (human)
cytosolInositol hexakisphosphate kinase 1Homo sapiens (human)
nucleusInositol hexakisphosphate kinase 1Homo sapiens (human)
cytoplasmInositol hexakisphosphate kinase 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (13)

Assay IDTitleYearJournalArticle
AID1809927Induction of drug resistance in Candida glabrata BG2 assessed as increase in ECZ IC50 at 8 times IC50 after 4 days2021Journal of medicinal chemistry, 11-11, Volume: 64, Issue:21
Optimization and Evaluation of Novel Antifungal Agents for the Treatment of Fungal Infection.
AID1809933Induction of drug resistant in Candida albicans ATCC SC5314 assessed as increase in EZC IC50 at 16 times IC502021Journal of medicinal chemistry, 11-11, Volume: 64, Issue:21
Optimization and Evaluation of Novel Antifungal Agents for the Treatment of Fungal Infection.
AID1872540Plasma protein binding in human2022European journal of medicinal chemistry, Mar-05, Volume: 231Synthetic approaches and structural diversity of triazolylbutanols derived from voriconazole in the antifungal drug development.
AID1809901Fungicidal activity against Cryptococcus neoformans H99 at 8 times of MIC after 24 hrs by time-kill kinetics assay2021Journal of medicinal chemistry, 11-11, Volume: 64, Issue:21
Optimization and Evaluation of Novel Antifungal Agents for the Treatment of Fungal Infection.
AID1809932Induction of drug resistance in Candida albicans ATCC SC5314 assessed as increase in EZC IC50 at 8 time IC50 after 35 days2021Journal of medicinal chemistry, 11-11, Volume: 64, Issue:21
Optimization and Evaluation of Novel Antifungal Agents for the Treatment of Fungal Infection.
AID1809934Induction of drug resistant in Candida glabrata BG2 assessed as increase in EZC IC50 at 16 times IC502021Journal of medicinal chemistry, 11-11, Volume: 64, Issue:21
Optimization and Evaluation of Novel Antifungal Agents for the Treatment of Fungal Infection.
AID1809952Ex vivo antifungal activity against Trichophyton rubrum KCCM60450 infected in human nail assessed as reduction in ATP level at 10 % w/w after 24 hrs2021Journal of medicinal chemistry, 11-11, Volume: 64, Issue:21
Optimization and Evaluation of Novel Antifungal Agents for the Treatment of Fungal Infection.
AID1809925Induction of drug resistance in Candida albicans ATCC SC5314 assessed as increase in EZC IC50 at 8 time IC50 after 7 days2021Journal of medicinal chemistry, 11-11, Volume: 64, Issue:21
Optimization and Evaluation of Novel Antifungal Agents for the Treatment of Fungal Infection.
AID1296008Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening2020SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1
Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID1346986P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1346987P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1347159Primary screen GU Rhodamine qHTS for Zika virus inhibitors: Unlinked NS2B-NS3 protease assay2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347160Primary screen NINDS Rhodamine qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (128)

TimeframeStudies, This Drug (%)All Drugs %
pre-19900 (0.00)18.7374
1990's0 (0.00)18.2507
2000's4 (3.13)29.6817
2010's84 (65.63)24.3611
2020's40 (31.25)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 57.27

According to the monthly volume, diversity, and competition of internet searches for this compound, as well the volume and growth of publications, there is estimated to be very strong demand-to-supply ratio for research on this compound.

MetricThis Compound (vs All)
Research Demand Index57.27 (24.57)
Research Supply Index5.08 (2.92)
Research Growth Index6.45 (4.65)
Search Engine Demand Index127.05 (26.88)
Search Engine Supply Index2.81 (0.95)

This Compound (57.27)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials24 (17.65%)5.53%
Reviews22 (16.18%)6.00%
Case Studies11 (8.09%)4.05%
Observational0 (0.00%)0.25%
Other79 (58.09%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (6)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Evaluating the Efficacy and Compatibility of Efinaconazole 10% Solution (Jublia) for the Treatment of Toenail Onychomycosis in Patients Wearing Toenail Polish Compared to Those Without Polish [NCT03110029]Phase 413 participants (Actual)Interventional2015-09-30Completed
A Multicenter, Open Label, Single-arm Study Evaluating the Safety and Pharmacokinetics of Efinaconazole Topical Solution in Subjects With Mild to Severe Onychomycosis of the Toenails [NCT02812771]Phase 462 participants (Actual)Interventional2016-08-04Completed
An Investigator Initiated Pilot Study Evaluating the Efficacy of Efinaconazole 10% Solution (Jublia) for the Treatment of Onychomycosis With Dermatophytomas [NCT03098615]Phase 419 participants (Actual)Interventional2015-09-30Completed
Real-World Evaluation of the Effect of Jublia on Nail Polish [NCT03022916]5 participants (Actual)Interventional2015-09-30Completed
Efficacy and Safety of Efinaconazole 10% Solution in the Treatment of Onychomycosis in Diabetic Patients [NCT03168841]Phase 340 participants (Actual)Interventional2017-06-06Completed
A Multicenter, Open-label, Non-controlled, Single-arm Phase IV Clinical Trial to Evaluate the Efficacy and Safety of Jublia® in Mild to Moderate Toenail Onychomycosis [NCT03280927]Phase 497 participants (Actual)Interventional2017-11-10Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT02812771 (1) [back to overview]Percentage of Participants With at Least One Adverse Event
NCT03022916 (1) [back to overview]Observe Stability of Nail Polish as Evidenced by Serial Photography With Efinaconazole Application in Terms of Days
NCT03098615 (2) [back to overview]Clinical or Mycological Cure of Nail
NCT03098615 (2) [back to overview]Number of Participants With Elimination of Dermatophytomas That Occur in Distal Lateral Subungual Onychomycosis (DLSO)
NCT03110029 (2) [back to overview]Percentage of Disease Improvement Using Onychomycosis Severity Index (OSI)
NCT03110029 (2) [back to overview]Percentage of Nail Polish Disruption Using the Likert Scale
NCT03168841 (4) [back to overview]Primary Endpoint - Efficacy
NCT03168841 (4) [back to overview]Secondary Endpoint - Efficacy
NCT03168841 (4) [back to overview]Secondary Endpoint - Efficacy
NCT03168841 (4) [back to overview]Secondary Endpoint - Safety (Occurrence of Adverse Events: Type and Frequency)

Percentage of Participants With at Least One Adverse Event

(NCT02812771)
Timeframe: 48 weeks

InterventionParticipants (Count of Participants)
Efinaconazole39

[back to top]

Observe Stability of Nail Polish as Evidenced by Serial Photography With Efinaconazole Application in Terms of Days

Observation: Serial photographs were combined with patient reported outcomes to assess the stability of self-applied toenail polish when efinaconazole was applied topically to the nail. (Expected stability of polish less than 14 days with application of Jublia as compared to nails without Jublia application) (NCT03022916)
Timeframe: Baseline to 14 days

Interventiondays of stability (Median)
Nail Polish and Efinaconazole Solution1.5
Efinaconazole Solution, Nail Polish, and Top Coat5
Placebo Comparator: Nail Polish Only15
Base Coat + Nail Polish + Top Coat + Efinaconazole Solution5

[back to top]

Clinical or Mycological Cure of Nail

Completely normal nail plate or negative fungal culture (NCT03098615)
Timeframe: week 48

InterventionParticipants (Count of Participants)
Jublia (Efinaconazole 10% Topical Solution) + Nail Polish12

[back to top]

Number of Participants With Elimination of Dermatophytomas That Occur in Distal Lateral Subungual Onychomycosis (DLSO)

Clear nail growth between the proximal nail fold and the dermatophytoma's proximal edge will be measured. (NCT03098615)
Timeframe: week 48

InterventionParticipants (Count of Participants)
Baseline Group19

[back to top]

Percentage of Disease Improvement Using Onychomycosis Severity Index (OSI)

Using 3rd party blinding, DLSO was assessed at baseline and at every subsequent visit using the onychomycosis severity index (OSI), measuring percent of the target nail involved, and grading the infection from mild to moderate to severe. The range for OSI is 0-20 with 20 indicating severe nails disease. Nail growth was measured at each visit. Fungal testing was done at screening, 3 months, 7 months, end of treatment (48 weeks), and end of study (52 weeks). Clinical and mycologic cure was evaluated at week 52. (NCT03110029)
Timeframe: 52 week

Interventionpercentage change target nail (Mean)
Wearing Toenail Polish0.56
Abstain From Wearing Toenail Polish0.54

[back to top]

Percentage of Nail Polish Disruption Using the Likert Scale

"Patients will answer the following question:~Which will be answered using a Likert scale where 0 represents no alteration in polish and 10 represents complete destruction of the polish:~Is the quality of your polish diminished with use of Jublia?" (NCT03110029)
Timeframe: 52 weeks

Interventionpercentage of nail polish disruption (Mean)
Wearing Toenail Polish0.6
Abstain From Wearing Toenail Polish0

[back to top]

Primary Endpoint - Efficacy

The primary efficacy end point is the proportion of subjects achieving complete cure at week 50. Complete cure is to be defined as a combination of 0% clinical involvement and mycological cure (mycological cure defined as negative KOH examination and negative fungal culture of the target toenail sample). (NCT03168841)
Timeframe: 50 weeks

InterventionParticipants (Count of Participants)
Intervention Group, Receiving Medication4

[back to top]

Secondary Endpoint - Efficacy

The first secondary efficacy end point is mycological cure, defined as negative KOH examination and negative fungal culture of the target toenail sample. (NCT03168841)
Timeframe: 50 weeks

InterventionParticipants (Count of Participants)
Intervention Group, Receiving Medication21

[back to top]

Secondary Endpoint - Efficacy

The second secondary efficacy end point is clinical cure, defined as 0% clinical involvement of the target toenail. (NCT03168841)
Timeframe: 50 weeks

InterventionParticipants (Count of Participants)
Intervention Group, Receiving Medication8

[back to top]

Secondary Endpoint - Safety (Occurrence of Adverse Events: Type and Frequency)

The secondary safety endpoint is the occurrence of adverse events (type and frequency). (NCT03168841)
Timeframe: 50 weeks

InterventionParticipants (Count of Participants)
Intervention Group, Receiving Medication4

[back to top]