Compounds > ipragliflozin
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ipragliflozin

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Cross-References

ID SourceID
PubMed CID10453870
CHEMBL ID2018096
CHEBI ID134724
SCHEMBL ID337645
MeSH IDM0574629

Synonyms (44)

Synonym
CHEBI:134724
ipragliflozin ,
D10196
ipragliflozin (inn)
bdbm50381554
asp-1941
asp1941
ipragliflozin [inn]
3n2n8oor7x ,
761423-87-4
asp 1941
suglat
(1s)-1,5-anhydro-1-c-(3-((1-benzothiophen-2-yl)methyl)-4-fluorophenyl)-d-glucitol
(1s)-1,5-anhydro-1-(3-(1-benzothiophen-2-ylmethyl)-4-fluorophenyl)-d-glucitol
unii-3n2n8oor7x
ipragliflozin [who-dd]
ipragliflozin [mi]
d-glucitol, 1,5-anhydro-1-c-(3-(benzo(b)thien-2-ylmethyl)-4-fluorophenyl)-, (1s)-
CHEMBL2018096 ,
S8637
HY-14894
SCHEMBL337645
AHFWIQIYAXSLBA-RQXATKFSSA-N
(1s)-1,5-anhydro-1-[3-(1-benzothien-2-ylmethyl)-4-fluorophenyl]-d-glucitol
(1s)-1,5-anhydro-1-c-[3-(1-benzothiophene-2-ylmethyl)-4-fluorophenyl]-d-glucitol
gtpl9394
(2s,3r,4r,5s,6r)-2-(3-(benzo[b]thiophen-2-ylmethyl)-4-fluorophenyl)-6-(hydroxymethyl)tetrahydro-2h-pyran-3,4,5-triol
AC-29008
AKOS025405258
(2s,3r,4r,5s,6r)-2-[3-(1-benzothiophen-2-ylmethyl)-4-fluorophenyl]-6-(hydroxymethyl)oxane-3,4,5-triol
(2s,3r,4r,5s,6r)-2-{3-[(1-benzothiophen-2-yl)methyl]-4-fluorophenyl}-6-(hydroxymethyl)oxane-3,4,5-triol
(1s)-1,5-anhydro-1-c-[3-[(1-benzothiophen-2-yl)methyl]-4-fluorophenyl]-d-glucitol
ipragliflozin (asp1941)
EX-A2770
DB11698
AS-39358
Q17193526
d-glucitol,1,5-anhydro-1-c-[3-(benzo[b]thien-2-ylmethyl)-4-fluorophenyl]-, (1s)-
ipragliflozin-l-proline
AMY38779
CCG-268693
NCGC00378606-02
d-glucitol, 1,5-anhydro-1-c-[3-(benzo[b]thien-2-ylmethyl)-4-fluorophenyl]-, (1s)-; (1s)-1,5-anhydro-1-c-[3-(benzo[b]thien-2-ylmethyl)-4-fluorophenyl]-d-glucitol; asp 1941; ipragliflozin; suglat
DTXSID701032738

Research Excerpts

Overview

Ipragliflozin is an SGLT2 inhibitor approved in Japan in combination with insulin for patients with T1D. It is a new antidiabetic agent that works through enhancing renal glucose excretion.

ExcerptReferenceRelevance
"Ipragliflozin is an SGLT2 inhibitor approved in Japan in combination with insulin for patients with T1D."( Overlapping risk factors for diabetic ketoacidosis in patients with type 1 diabetes on ipragliflozin: case analysis of spontaneous reports in Japan from a pharmacovigilance safety database.
Abiru, N; Nakatsuji, Y; Noguchi, M; Tsuboi, K, )		1.08
"Ipragliflozin is a potent, selective SGLT-2 inhibitor used for the management of type 2 diabetes."( Profile of Ipragliflozin, an Oral SGLT-2 Inhibitor for the Treatment of Type 2 Diabetes: The Evidence to Date.
Alkabbani, W; Gamble, JM, 2021)		1.73
"Ipragliflozin is a useful oral antidiabetic medication for patients with a wide range of background characteristics."( Efficacy of ipragliflozin as monotherapy or as add-on therapy with other oral antidiabetic medications for treating type 2 diabetes in Japanese patients with inadequate glycemic control: A subgroup analysis based on patient characteristics.
Ishida, H; Nakamoto, S; Osonoi, T; Osonoi, Y; Saito, M; Tamasawa, A, 2018)		2.3
"Ipragliflozin is a selective sodium glucose cotransporter 2 (SGLT2) inhibitor that increases urinary glucose excretion and subsequently improves hyperglycemia in patients with type 2 diabetes mellitus (T2DM). "( Protective Effect of Ipragliflozin on Pancreatic Islet Cells in Obese Type 2 Diabetic db/db Mice.
Takakura, S; Takasu, T, 2018)		2.24
"Ipragliflozin is a new antidiabetic agent that works through enhancing renal glucose excretion. "( Tolerability and Efficacy of Ipragliflozin in The Management of Inadequately Controlled Type 2 Diabetes mellitus: A Systematic Review and Meta-analysis.
Abdelazeim, B; Abdelazeim, N; El Ashal, G; Elgebaly, A; Mattar, O; Namous, L; Nasreldin, N, 2021)		2.36
"Ipragliflozin is an SGLT2 inhibitor in Phase 3 clinical development for the treatment of type 2 diabetes mellitus (T2DM)."( Ipragliflozin and other sodium-glucose cotransporter-2 (SGLT2) inhibitors in the treatment of type 2 diabetes: preclinical and clinical data.
Kurosaki, E; Ogasawara, H, 2013)		2.55
"Ipragliflozin is a novel and selective sodium-glucose cotransporter 2 (SGLT2) inhibitor that induces sustained increases in urinary glucose excretion by inhibiting renal glucose reabsorption and thereby exerting a subsequent antihyperglycemic effect. "( SGLT2 selective inhibitor ipragliflozin reduces body fat mass by increasing fatty acid oxidation in high-fat diet-induced obese rats.
Hayashizaki, Y; Kihara, R; Kurosaki, E; Li, Q; Mitsuoka, K; Miyoshi, S; Muramatsu, Y; Sasamata, M; Shibasaki, M; Tahara, A; Takasu, T; Tomiyama, H; Uchiyama, Y; Yokono, M, 2014)		2.15
"Ipragliflozin is a novel and highly selective sodium-glucose transporter 2 (SGLT2) inhibitor that reduces plasma glucose levels by enhancing urinary glucose excretion in patients with type 2 diabetes mellitus (T2DM). "( Pharmacokinetic and pharmacodynamic study of ipragliflozin in Japanese patients with type 2 diabetes mellitus: a randomized, double-blind, placebo-controlled study.
Akiyama, N; Kadokura, T; Kageyama, S; Kashiwagi, A; Kazuta, K; Nagase, I; Smulders, R; Utsuno, A; Yoshida, S, 2014)		2.1
"Ipragliflozin (Suglat(®)) is a potent and selective inhibitor of sodium-glucose cotransporter-2 that was recently launched in Japan. "( Clinical pharmacokinetics and pharmacodynamics of the novel SGLT2 inhibitor ipragliflozin.
Kadokura, T; Keirns, J; Krauwinkel, W; Leeflang, S; Nakajo, I; Smulders, R; Taniuchi, Y; Zhang, W, 2014)		2.07
"Ipragliflozin is a valid treatment option for patients with mild RI but not those with moderate RI."( A randomized, double-blind, placebo-controlled study on long-term efficacy and safety of ipragliflozin treatment in patients with type 2 diabetes mellitus and renal impairment: results of the long-term ASP1941 safety evaluation in patients with type 2 dia
Ishikawa, H; Kashiwagi, A; Kazuta, K; Takahashi, H; Ueyama, E; Utsuno, A; Yoshida, S, 2015)		1.36
"Ipragliflozin is a selective sodium glucose cotransporter 2 (SGLT2) inhibitor that increases urinary glucose excretion by inhibiting renal glucose reabsorption and thereby causes a subsequent antihyperglycemic effect. "( Ipragliflozin, an SGLT2 inhibitor, exhibits a prophylactic effect on hepatic steatosis and fibrosis induced by choline-deficient l-amino acid-defined diet in rats.
Hayashizaki-Someya, Y; Koide, K; Kurosaki, E; Mitori, H; Takakura, S; Takasu, T; Yamazaki, S, 2015)		3.3
"Ipragliflozin is a highly potent and selective sodium-dependent glucose co-transporter-2 (SGLT2) inhibitor, a novel class of hypoglycemic agents. "( A quantitative LC-MS/MS method for determining ipragliflozin, a sodium-glucose co-transporter 2 (SGLT-2) inhibitor, and its application to a pharmacokinetic study in rats.
Ito, Y; Kobuchi, S; Sakaeda, T; Yano, K, 2015)		2.12
"Ipragliflozin is a novel selective sodium-dependent glucose cotransporter 2 inhibitor of urinary glucose excretion."( [Efficacy of Ipragliflozin in Patients with Steroid-Induced Hyperglycemia during Cancer Chemotherapy].
Bando, H; Horasawa, S; Kawasumi, K; Ohashi, K; Osame, K; Saito, S, 2016)		1.52
"Ipragliflozin is a new drug for the treatment of diabetes mellitus. "( First case of drug eruption due to ipragliflozin: Case report and review of the literature.
Nakamura, M; Nishio, D; Saito-Sasaki, N; Sawada, Y, 2017)		2.17
"Ipragliflozin (ASP1941) is a novel, selective inhibitor of the sodium-dependent glucose co-transporter 2, which is highly expressed in the proximal tubules of the kidneys."( Effect of Ipragliflozin (ASP1941), a novel selective sodium-dependent glucose co-transporter 2 inhibitor, on urinary glucose excretion in healthy subjects.
Kadokura, T; Krauwinkel, WJ; Smulders, RA; Veltkamp, SA, 2011)		1.49
"Ipragliflozin (ASP1941) is a selective sodium glucose cotransporter 2 inhibitor in clinical development for the treatment of patients with type 2 diabetes mellitus (T2DM)."( Combination treatment with ipragliflozin and metformin: a randomized, double-blind, placebo-controlled study in patients with type 2 diabetes mellitus.
Collins, C; Kadokura, T; Smulders, RA; van Bruijnsvoort, M; van Dijk, J; Veltkamp, SA, 2012)		2.12
"Ipragliflozin is a novel, selective inhibitor of sodium glucose co-transporter 2 (SGLT2 inhibitor) in clinical development for type 2 diabetes mellitus (T2DM) treatment. "( Efficacy and safety of ipragliflozin in patients with type 2 diabetes inadequately controlled on metformin: a dose-finding study.
Dhanjal, P; Ferrannini, E; Fonseca, VA; Houzer, A; Wilding, JP; Wilpshaar, W, 2013)		2.14

Effects

ExcerptReferenceRelevance
"Ipragliflozin has a favourable safety profile with a low risk of hypoglycemia and the rates of common adverse events are not significantly different than placebo."( Profile of Ipragliflozin, an Oral SGLT-2 Inhibitor for the Treatment of Type 2 Diabetes: The Evidence to Date.
Alkabbani, W; Gamble, JM, 2021)		1.73

Treatment

Ipragliflozin treatment markedly attenuated HFD-induced hepatic steatosis and reduced the size of hypertrophied adipocytes to that of smaller adipocytes. Treatment with ipraglif lozin increased urinary glu.

ExcerptReferenceRelevance
"Ipragliflozin treatment was also associated with sustained improvements in efficacy parameters for over 3 years."( Real-World Evidence for Long-Term Safety and Effectiveness of Ipragliflozin in Japanese Patients with Type 2 Diabetes Mellitus: final Results of a 3-Year Post-Marketing Surveillance Study (STELLA-LONG TERM).
Maegawa, H; Nakamura, I; Tobe, K; Uno, S, 2021)		1.58
"Ipragliflozin treatment markedly attenuated HFD-induced hepatic steatosis and reduced the size of hypertrophied adipocytes to that of smaller adipocytes."( Ipragliflozin, an SGLT2 Inhibitor, Ameliorates High-Fat Diet-Induced Metabolic Changes by Upregulating Energy Expenditure through Activation of the AMPK/ SIRT1 Pathway.
Bae, J; Cha, BS; Kang, ES; Lee, BW; Lee, JY; Lee, M; Lee, YH; Shin, E, 2021)		2.79
"Ipragliflozin treatment resulted in statistically significant improvements versus baseline in hemoglobin A1c, fasting plasma glucose concentration, body weight, blood pressure, heart rate, and serum concentrations of low-density lipoprotein cholesterol and triglycerides."( Safety and efficacy of ipragliflozin in Japanese patients with type 2 diabetes in real-world clinical practice: interim results of the STELLA-LONG TERM post-marketing surveillance study.
Maegawa, H; Nakamura, I; Tabuchi, H; Tobe, K; Uno, S, 2018)		1.51
"More ipragliflozin-treated patients than placebo-treated patients achieved HbA1c target levels of <7.0% (44.4% vs 12.1%) and < 6.5% (12.5% vs 1.5%) at EOT (P < .05 for both)."( Efficacy and safety of ipragliflozin as an add-on therapy to sitagliptin and metformin in Korean patients with inadequately controlled type 2 diabetes mellitus: A randomized controlled trial.
Baik, S; Cha, BS; Chon, S; Chung, CH; Han, KA; Jung, CH; Kim, DS; Lee, IK; Lee, KW; Lee, MK; Lim, S; Park, KS; Park, S; Sakatani, T; Yoon, KH, 2018)		1.25
"Ipragliflozin treatment for 24 weeks resulted in reduced BW, mainly from fat mass loss. "( Ipragliflozin, a sodium-glucose cotransporter 2 inhibitor, reduces bodyweight and fat mass, but not muscle mass, in Japanese type 2 diabetes patients treated with insulin: A randomized clinical trial.
Arima, H; Fuse, K; Ida, S; Inoue, H; Kondo, K; Maegawa, H; Miura, K; Miyazawa, I; Morino, K; Murata, K; Ohashi, N; Sato, D; Sekine, O; Tanaka-Mizuno, S; Ugi, S; Yoshimura, M, 2019)		3.4
"Ipragliflozin is a valid treatment option for patients with mild RI but not those with moderate RI."( A randomized, double-blind, placebo-controlled study on long-term efficacy and safety of ipragliflozin treatment in patients with type 2 diabetes mellitus and renal impairment: results of the long-term ASP1941 safety evaluation in patients with type 2 dia
Ishikawa, H; Kashiwagi, A; Kazuta, K; Takahashi, H; Ueyama, E; Utsuno, A; Yoshida, S, 2015)		1.36
"Ipragliflozin treatment improved glycaemic control when added to metformin therapy and may be associated with weight loss and reductions in blood pressure compared to placebo. "( Efficacy and safety of ipragliflozin in patients with type 2 diabetes inadequately controlled on metformin: a dose-finding study.
Dhanjal, P; Ferrannini, E; Fonseca, VA; Houzer, A; Wilding, JP; Wilpshaar, W, 2013)		2.14
"Treatment with ipragliflozin increased urinary glucose excretion, reduced hemoglobin A1c (HbA1c) levels and suppressed body weight gain as the dose increased."( The Sodium Glucose Cotransporter 2 Inhibitor Ipragliflozin Promotes Preferential Loss of Fat Mass in Non-obese Diabetic Goto-Kakizaki Rats.
Amino, N; Hayashizaki, Y; Hirosumi, J; Kurosaki, E; Minoura, H; Takakura, S; Takasu, T, 2017)		1.05
"Treatment with ipragliflozin may protect against the progressive loss of islet β-cells in patients with T2DM."( Protective Effect of Ipragliflozin on Pancreatic Islet Cells in Obese Type 2 Diabetic db/db Mice.
Takakura, S; Takasu, T, 2018)		1.14
"Treatment of ipragliflozin (10mg/kg once daily) reduced body weight despite a slight increase in food intake."( SGLT2 selective inhibitor ipragliflozin reduces body fat mass by increasing fatty acid oxidation in high-fat diet-induced obese rats.
Hayashizaki, Y; Kihara, R; Kurosaki, E; Li, Q; Mitsuoka, K; Miyoshi, S; Muramatsu, Y; Sasamata, M; Shibasaki, M; Tahara, A; Takasu, T; Tomiyama, H; Uchiyama, Y; Yokono, M, 2014)		1.06
"Treatment with ipragliflozin, an SGLT2 inhibitor, improved HbA1c from 8.4% to 6.0% and glycated albumin from 29.4% to 17.9%."( SGLT2 inhibitors provide an effective therapeutic option for diabetes complicated with insulin antibodies.
Hayashi, A; Kawai, S; Shichiri, M; Takano, K, 2016)		0.77
"Treatment with ipragliflozin reduced glycated hemoglobin levels, inhibited the progression of cataract formation, prevented the prolongation of oscillatory potential peaks in the electroretinogram, ameliorated the slowing of motor nerve conduction velocity, and reduced the severity of glomerulosclerosis in SDT fatty rats."( Effect of ipragliflozin, an SGLT2 inhibitor, on progression of diabetic microvascular complications in spontaneously diabetic Torii fatty rats.
Hayashizaki, Y; Takakura, S; Takasu, T; Toyoshi, T, 2016)		1.19
"Treatment with ipragliflozin markedly attenuated the development of liver fibrosis and expression of hepatic fibrosis markers, such as alpha smooth muscle actin, collagen 1A1, and transforming growth factor beta (TGF-β), and improved IR in a dose-dependent manner in OLETF rats."( Ipragliflozin, a sodium-glucose cotransporter 2 inhibitor, ameliorates the development of liver fibrosis in diabetic Otsuka Long-Evans Tokushima fatty rats.
Aihara, Y; Asada, K; Douhara, A; Kawaratani, H; Kitade, M; Moriya, K; Namisaki, T; Nishimura, N; Noguchi, R; Okura, Y; Takeda, K; Yoshiji, H, 2016)		2.22
"Treatment with ipragliflozin for 12 weeks significantly decreased fasting glucose, HbA1c, and blood pressure levels without severe adverse events. "( Predictors of response to ipragliflozin treatment in patients with type 2 diabetes mellitus.
Ebihara, K; Ishibashi, S; Kotani, K; Okada, K; Yamazaki, H, 2016)		1.09

Toxicity

The most common treatment-emergent adverse events (ipragliflozin vs placebo) were upper respiratory tract infection. The incidences of treatment-Emergent Adverse Events were similar between the ipraglif lozin and placebo groups in all patients combined.

ExcerptReferenceRelevance
"The incidence of treatment-emergent adverse events was similar for placebo and ipragliflozin groups."( Safety, pharmacokinetic, and pharmacodynamic profiles of ipragliflozin (ASP1941), a novel and selective inhibitor of sodium-dependent glucose co-transporter 2, in patients with type 2 diabetes mellitus.
Akinlade, B; Klasen, S; Kowalski, D; Schwartz, SL; Wilpshaar, W; Zhang, W, 2011)		0.84
" Adverse events (AEs), vital signs and laboratory safety measurements were assessed."( Efficacy and safety of ipragliflozin in patients with type 2 diabetes inadequately controlled on metformin: a dose-finding study.
Dhanjal, P; Ferrannini, E; Fonseca, VA; Houzer, A; Wilding, JP; Wilpshaar, W, 2013)		0.7
" Proportions of patients experiencing treatment-emergent adverse events were similar across all groups: ipragliflozin (45."( Active- and placebo-controlled dose-finding study to assess the efficacy, safety, and tolerability of multiple doses of ipragliflozin in patients with type 2 diabetes mellitus.
Ball, G; Dhanjal, P; Ferrannini, E; Fonseca, VA; Klasen, S; Wilding, JP; Wilpshaar, W, )		0.55
" Outcomes included the changes in hemoglobin A1c, fasting plasma glucose, bodyweight and treatment-emergent adverse events."( Efficacy and safety of ipragliflozin in Japanese patients with type 2 diabetes stratified by body mass index: A subgroup analysis of five randomized clinical trials.
Kashiwagi, A; Kawamuki, K; Kazuta, K; Kosakai, Y; Nakamura, I; Satomi, H; Takahashi, H; Ueyama, E; Yoshida, S, 2016)		0.74
" The incidences of treatment-emergent adverse events were similar between the ipragliflozin and placebo groups in all patients combined and in the four body mass index categories."( Efficacy and safety of ipragliflozin in Japanese patients with type 2 diabetes stratified by body mass index: A subgroup analysis of five randomized clinical trials.
Kashiwagi, A; Kawamuki, K; Kazuta, K; Kosakai, Y; Nakamura, I; Satomi, H; Takahashi, H; Ueyama, E; Yoshida, S, 2016)		0.97
" Safety outcomes included treatment-emergent adverse events."( Efficacy, safety, and tolerability of ipragliflozin in Asian patients with type 2 diabetes mellitus and inadequate glycemic control with metformin: Results of a phase 3 randomized, placebo-controlled, double-blind, multicenter trial.
Cha, BS; Chuang, LM; Kokubo, S; Lu, CH; Min, KW; Yoshida, S, 2016)		0.71
" The most common treatment-emergent adverse events (ipragliflozin vs placebo) were upper respiratory tract infection (9."( Efficacy, safety, and tolerability of ipragliflozin in Asian patients with type 2 diabetes mellitus and inadequate glycemic control with metformin: Results of a phase 3 randomized, placebo-controlled, double-blind, multicenter trial.
Cha, BS; Chuang, LM; Kokubo, S; Lu, CH; Min, KW; Yoshida, S, 2016)		0.96
" Hypoglycaemia was the only treatment-related adverse event reported in >5% of patients (14."( Efficacy and safety of ipragliflozin as add-on therapy to insulin in Japanese patients with type 2 diabetes mellitus (IOLITE): a multi-centre, randomized, placebo-controlled, double-blind study.
Asahina, S; Ishihara, H; Nakao, I; Okitsu, A; Yamaguchi, S, 2016)		0.74
"Changes in glycemic control, blood pressure, and laboratory variables from baseline, and incidence of adverse drug reactions (ADRs)."( Baseline characteristics and interim (3-month) efficacy and safety data from STELLA-LONG TERM, a long-term post-marketing surveillance study of ipragliflozin in Japanese patients with type 2 diabetes in real-world clinical practice.
Maegawa, H; Nakamura, I; Tabuchi, H; Tobe, K, 2016)		0.63
" Survey items included demographics, treatments, adverse drug reactions (ADRs), vital signs, and laboratory variables."( Real-world evidence for the safety of ipragliflozin in elderly Japanese patients with type 2 diabetes mellitus (STELLA-ELDER): final results of a post-marketing surveillance study.
Nakamura, I; Sugamori, H; Terauchi, Y; Yokote, K, 2016)		0.71
" The adverse drug reaction incidence rate was 10."( Safety and efficacy of ipragliflozin in Japanese patients with type 2 diabetes in real-world clinical practice: interim results of the STELLA-LONG TERM post-marketing surveillance study.
Maegawa, H; Nakamura, I; Tabuchi, H; Tobe, K; Uno, S, 2018)		0.79
" In this subgroup analysis, patient characteristics, laboratory variables, and adverse drug reactions (ADRs) were compared between non-elderly (<65 years) and elderly (≥65 years) patients."( Safety and efficacy of ipragliflozin in elderly versus non-elderly Japanese patients with type 2 diabetes mellitus: a subgroup analysis of the STELLA-LONG TERM study.
Maegawa, H; Nakamura, I; Tabuchi, H; Tobe, K; Uno, S, 2018)		0.79
" Adverse event rates were similar between groups (ipragliflozin: 51."( Efficacy and safety of ipragliflozin as an add-on therapy to sitagliptin and metformin in Korean patients with inadequately controlled type 2 diabetes mellitus: A randomized controlled trial.
Baik, S; Cha, BS; Chon, S; Chung, CH; Han, KA; Jung, CH; Kim, DS; Lee, IK; Lee, KW; Lee, MK; Lim, S; Park, KS; Park, S; Sakatani, T; Yoon, KH, 2018)		1.04
" The incidence of adverse drug reactions was evaluated as a safety end-point."( Safety and efficacy of tofogliflozin in Japanese patients with type 2 diabetes mellitus in real-world clinical practice: Results of 3-month interim analysis of a long-term post-marketing surveillance study (J-STEP/LT).
Fujii, S; Fujiwara, H; Gunji, R; Kakiuchi, S; Kaku, K; Kameda, H; Kurihara, Y; Senda, M; Tamura, M; Utsunomiya, K, 2019)		0.51
" Adverse drug reactions occurred in 345 of 6,712 patients (5."( Safety and efficacy of tofogliflozin in Japanese patients with type 2 diabetes mellitus in real-world clinical practice: Results of 3-month interim analysis of a long-term post-marketing surveillance study (J-STEP/LT).
Fujii, S; Fujiwara, H; Gunji, R; Kakiuchi, S; Kaku, K; Kameda, H; Kurihara, Y; Senda, M; Tamura, M; Utsunomiya, K, 2019)		0.51
" Adverse drug reactions were more common in patients with higher BMI than in those with lower BMI."( Impact of body mass index on the efficacy and safety of ipragliflozin in Japanese patients with type 2 diabetes mellitus: A subgroup analysis of 3-month interim results from the Specified Drug Use Results Survey of Ipragliflozin Treatment in Type 2 Diabet
Maegawa, H; Nakamura, I; Tabuchi, H; Tobe, K; Uno, S, 2019)		0.76
" The incidence of adverse drug reactions (ADRs) was evaluated for safety."( Safety and Effectiveness of Ipragliflozin for Type 2 Diabetes in Japan: 12-Month Interim Results of the STELLA-LONG TERM Post-Marketing Surveillance Study.
Maegawa, H; Nakamura, I; Tobe, K; Uno, S, 2019)		0.81
" However, wide CIs for many comparisons suggest limited precision, and therefore clinically important adverse events cannot be ruled out."( Comparative safety of the sodium glucose co-transporter 2 (SGLT2) inhibitors: a systematic review and meta-analysis.
Aubrey-Bassler, K; Chibrikov, E; Curnew, D; Donnan, JR; Gamble, JM; Grandy, CA; Hache, J; Johnston, K; Marra, CA; Nguyen, H; Swab, M, 2019)		0.51
" Treatment-emergent adverse events (TEAEs) were evaluated."( Efficacy and safety of ipragliflozin add-on therapy to insulin in Japanese patients with type 1 diabetes mellitus: A randomized, double-blind, phase 3 trial.
Isaka, H; Kaku, K; Sakatani, T; Toyoshima, J, 2019)		0.82
" Safety outcomes were monitored as treatment-emergent adverse events."( Long-term (52-week) efficacy and safety of ipragliflozin add-on therapy to insulin in Japanese patients with type 1 diabetes mellitus: An uncontrolled, open-label extension of a phase III study.
Isaka, H; Kaku, K; Sakatani, T; Toyoshima, J, 2020)		0.82
" No serious drug-related treatment-emergent adverse events or deaths were reported."( Long-term (52-week) efficacy and safety of ipragliflozin add-on therapy to insulin in Japanese patients with type 1 diabetes mellitus: An uncontrolled, open-label extension of a phase III study.
Isaka, H; Kaku, K; Sakatani, T; Toyoshima, J, 2020)		0.82
" Whereas, several adverse events caused by SGLT2is were also reported."( Investigation of efficacy and safety of low-dose sodium glucose transporter 2 inhibitors and differences between two agents, canagliflozin and ipragliflozin, in patients with type 2 diabetes mellitus.
Abe, I; Abe, M; Fujii, H; Kobayashi, K; Kudo, T; Minezaki, M; Mukoubara, S; Ochi, K; Ohe, K; Ohishi, H; Ohnishi, Y; Shinagawa, T; Sugimoto, K; Takashi, Y; Yamao, Y, 2019)		0.71
" Survey items included demographics, treatments, adverse drug reactions (ADRs), vital signs, and laboratory variables."( Real-World Evidence for Long-Term Safety and Effectiveness of Ipragliflozin in Japanese Patients with Type 2 Diabetes Mellitus: final Results of a 3-Year Post-Marketing Surveillance Study (STELLA-LONG TERM).
Maegawa, H; Nakamura, I; Tobe, K; Uno, S, 2021)		0.86
" In Trial 843, the incidences of adverse events (AEs) overall and prespecified AEs of clinical interest (symptomatic hypoglycaemia, urinary tract infection, genital infection, hypovolaemia, and polyuria/pollakiuria) were similar between groups."( Efficacy and safety of ipragliflozin in Japanese patients with type 2 diabetes and inadequate glycaemic control on sitagliptin.
Engel, SS; Kadowaki, T; Kaku, K; Kaufman, KD; O'Neill, EA; Okamoto, T; Sato, A; Seino, Y; Shirakawa, M, 2021)		0.93
"Spontaneous safety reports of ipragliflozin adverse drug reactions (ADRs) in patients with T1D were collected during early post-marketing phase vigilance (EPPV; 21 December 2018-20 June 2019)."( Overlapping risk factors for diabetic ketoacidosis in patients with type 1 diabetes on ipragliflozin: case analysis of spontaneous reports in Japan from a pharmacovigilance safety database.
Abiru, N; Nakatsuji, Y; Noguchi, M; Tsuboi, K, )		0.64

Pharmacokinetics

The aim of the present study was to establish a new highly sensitive and rapid liquid chromatography-tandem mass spectrometry (LC-MS/MS) method. We examined the pharmacokinetic and pharmacodynamic characteristics of two oral doses of ipragliflozin in Japanese patients with T2DM. No changes in elimination half-life and protein binding were found.

ExcerptReferenceRelevance
"This Phase 2, randomized, placebo-controlled study investigated the safety, tolerability, and pharmacokinetic and pharmacodynamic profiles of the novel oral SGLT2 inhibitor ipragliflozin (ASP1941) in T2DM patients."( Safety, pharmacokinetic, and pharmacodynamic profiles of ipragliflozin (ASP1941), a novel and selective inhibitor of sodium-dependent glucose co-transporter 2, in patients with type 2 diabetes mellitus.
Akinlade, B; Klasen, S; Kowalski, D; Schwartz, SL; Wilpshaar, W; Zhang, W, 2011)		0.81
" No changes in elimination half-life and protein binding of ipragliflozin were observed in moderate hepatic impairment subjects."( The effect of moderate hepatic impairment on the pharmacokinetics of ipragliflozin, a novel sodium glucose co-transporter 2 (SGLT2) inhibitor.
Kadokura, T; Keirns, J; Krauwinkel, WJ; Lasseter, KC; Plumb, L; Smulders, R; Townsend, RW; Ushigome, F; Zhang, W, 2013)		0.87
" We examined the pharmacokinetic and pharmacodynamic characteristics of two oral doses of ipragliflozin in Japanese patients with T2DM."( Pharmacokinetic and pharmacodynamic study of ipragliflozin in Japanese patients with type 2 diabetes mellitus: a randomized, double-blind, placebo-controlled study.
Akiyama, N; Kadokura, T; Kageyama, S; Kashiwagi, A; Kazuta, K; Nagase, I; Smulders, R; Utsuno, A; Yoshida, S, 2014)		0.88
" Plasma and urine pharmacodynamic parameters were measured on Days -1 and 14, and pharmacokinetic parameters on Day 14."( Pharmacokinetic and pharmacodynamic study of ipragliflozin in Japanese patients with type 2 diabetes mellitus: a randomized, double-blind, placebo-controlled study.
Akiyama, N; Kadokura, T; Kageyama, S; Kashiwagi, A; Kazuta, K; Nagase, I; Smulders, R; Utsuno, A; Yoshida, S, 2014)		0.66
" The aim of this review is to provide a comprehensive overview of currently available pharmacokinetic and pharmacodynamic data on ipragliflozin, including studies in healthy subjects, patients with type 2 diabetes mellitus and special populations."( Clinical pharmacokinetics and pharmacodynamics of the novel SGLT2 inhibitor ipragliflozin.
Kadokura, T; Keirns, J; Krauwinkel, W; Leeflang, S; Nakajo, I; Smulders, R; Taniuchi, Y; Zhang, W, 2014)		0.84
" The available SGLT2 inhibitors share similar pharmacokinetic characteristics, with a rapid oral absorption, a long elimination half-life allowing once-daily administration, an extensive hepatic metabolism mainly via glucuronidation to inactive metabolites, the absence of clinically relevant drug-drug interactions and a low renal elimination as parent drug."( Pharmacodynamics, efficacy and safety of sodium-glucose co-transporter type 2 (SGLT2) inhibitors for the treatment of type 2 diabetes mellitus.
Scheen, AJ, 2015)		0.42
" These SGLT2 inhibitors share similar pharmacokinetic characteristics with a rapid oral absorption, a long elimination half-life allowing once-daily administration, an extensive hepatic metabolism mainly via glucuronidation to inactive metabolites and a low renal elimination as a parent drug."( Pharmacokinetics, Pharmacodynamics and Clinical Use of SGLT2 Inhibitors in Patients with Type 2 Diabetes Mellitus and Chronic Kidney Disease.
Scheen, AJ, 2015)		0.42
" The aim of the present study was to establish a new highly sensitive and rapid liquid chromatography-tandem mass spectrometry (LC-MS/MS) method for the quantitative analysis of ipragliflozin in rat plasma and apply this method to a pharmacokinetic study in rats."( A quantitative LC-MS/MS method for determining ipragliflozin, a sodium-glucose co-transporter 2 (SGLT-2) inhibitor, and its application to a pharmacokinetic study in rats.
Ito, Y; Kobuchi, S; Sakaeda, T; Yano, K, 2015)		0.87
" Duration and onset of the pharmacologic effects seemed to be closely correlated with the pharmacokinetic properties of each SGLT2 inhibitor, particularly with respect to high distribution and long retention in the target organ, the kidney."( Characterization and comparison of sodium-glucose cotransporter 2 inhibitors in pharmacokinetics, pharmacodynamics, and pharmacologic effects.
Imamura, M; Kurosaki, E; Tahara, A; Takasu, T; Yokono, M, 2016)		0.43
"To characterize the pharmacokinetic and pharmacodynamic (PK/PD) relationship of ipragliflozin in Japanese patients with type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM) and to determine the appropriate dose regimen for a Phase III study of ipragliflozin in Japanese patients with T1DM."( Comparison of the Pharmacokinetic and Pharmacodynamic Relationship of Ipragliflozin Between Patients With Type 1 and Type 2 Diabetes Mellitus.
Isaka, H; Kaibara, A; Saito, M; Sakatani, T; Toyoshima, J, 2020)		1.02

Compound-Compound Interactions

There were no adverse effects on bone or muscle when sitagliptin was used in combination with either ipragliflozin or metformin.

ExcerptReferenceRelevance
"This multicenter, double-blind, placebo-controlled study examined the efficacy and safety of ipragliflozin, a sodium-glucose co-transporter 2 inhibitor, in combination with metformin in Japanese patients with type 2 diabetes mellitus (T2DM)."( Ipragliflozin in combination with metformin for the treatment of Japanese patients with type 2 diabetes: ILLUMINATE, a randomized, double-blind, placebo-controlled study.
Goto, K; Kashiwagi, A; Kazuta, K; Ueyama, E; Utsuno, A; Yoshida, S, 2015)		2.08
" Here, we investigated the antihyperglycemic effect of ipragliflozin, a selective sodium-glucose cotransporter 2 inhibitor, alone or in combination with oral antidiabetic drugs in a range of relevant mouse models to analyse the blood glucose-lowering properties of different drug types based on their mechanism of action."( Antihyperglycemic effect of ipragliflozin, a sodium-glucose co-transporter 2 inhibitor, in combination with oral antidiabetic drugs in mice.
Hayashizaki, Y; Kurosaki, E; Tahara, A; Takakura, S; Takasu, T, 2015)		0.96
"There were no adverse effects on bone or muscle when sitagliptin was used in combination with either ipragliflozin or metformin."( Effects of ipragliflozin versus metformin in combination with sitagliptin on bone and muscle in Japanese patients with type 2 diabetes mellitus: Subanalysis of a prospective, randomized, controlled study (PRIME-V study).
Baba, Y; Hashimoto, N; Hattori, A; Horikoshi, T; Ide, K; Ide, S; Ishibashi, R; Ishikawa, K; Ishikawa, T; Kitamoto, T; Kobayashi, A; Kobayashi, K; Koshizaka, M; Maezawa, Y; Nagashima, K; Nakamura, S; Newby, LK; Ogino, J; Ohara, E; Onishi, S; Sakamoto, K; Sato, Y; Shimada, F; Shimofusa, R; Shoji, M; Takahashi, S; Takemoto, M; Tokuyama, H; Uchida, D; Yamaga, M; Yokoh, H; Yokote, K, 2021)		1.23

Dosage Studied

The goal of this study was to assess the effect on cardiac repolarization (QTc interval) of repeated oral dosing of ipragliflozin at therapeutic (100 mg/d) and supratherapeutic (600 mg/D) levels in healthy subjects. Lower concentration of first-morning urine sodium and higher loop diuretic dosage were associated with urine volume increment.

ExcerptRelevanceReference
" Primary endpoints were the area under the curve from the time of dosing to infinity (AUC(inf)) and the maximum observed plasma concentration (C(max)) of each drug."( No pharmacokinetic interaction between ipragliflozin and sitagliptin, pioglitazone, or glimepiride in healthy subjects.
Kadokura, T; Keirns, J; Krauwinkel, WJ; Smulders, RA; van Dijk, J; Veltkamp, SA; Zhang, W, 2012)		0.65
" Once-daily dosing of ipragliflozin (0."( Antidiabetic effects of SGLT2-selective inhibitor ipragliflozin in streptozotocin-nicotinamide-induced mildly diabetic mice.
Hayashizaki, Y; Imamura, M; Kihara, R; Kobayashi, Y; Kurosaki, E; Noda, A; Qun, L; Sasamata, M; Shibasaki, M; Tahara, A; Takasu, T; Tomiyama, H; Yamajuku, D; Yokono, M, 2012)		0.95
"The goal of this study was to assess the effect on cardiac repolarization (QTc interval) of repeated oral dosing of ipragliflozin at therapeutic (100 mg/d) and supratherapeutic (600 mg/d) levels in healthy subjects."( Ipragliflozin does not prolong QTc interval in healthy male and female subjects: a phase I study.
Abeyratne, A; Dietz, A; Kadokura, T; Keirns, J; Krauwinkel, W; Smulders, R; Zhang, W, 2013)		2.04
" Thus, prescribing information should be consulted regarding dosage adjustments or restrictions in the case of renal dysfunction for each SGLT2 inhibitor."( Pharmacokinetics, Pharmacodynamics and Clinical Use of SGLT2 Inhibitors in Patients with Type 2 Diabetes Mellitus and Chronic Kidney Disease.
Scheen, AJ, 2015)		0.42
" The median dosing period was 320 days."( Effectiveness of Ipragliflozin, a Sodium-Glucose Co-transporter 2 Inhibitor, as a Second-line Treatment for Non-Alcoholic Fatty Liver Disease Patients with Type 2 Diabetes Mellitus Who Do Not Respond to Incretin-Based Therapies Including Glucagon-like Pep
Isogawa, A; Ohki, T; Tagawa, K; Toda, N, 2016)		0.77
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Drug Classes (1)

ClassDescription
glycosideA glycosyl compound resulting from the attachment of a glycosyl group to a non-acyl group RO-, RS-, RSe-, etc. The bond between the glycosyl group and the non-acyl group is called a glycosidic bond. By extension, the terms N-glycosides and C-glycosides are used as class names for glycosylamines and for compounds having a glycosyl group attached to a hydrocarbyl group respectively. These terms are misnomers and should not be used. The preferred terms are glycosylamines and C-glycosyl compounds, respectively.
[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 (2)

Inhibition Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Sodium/glucose cotransporter 1Homo sapiens (human)IC50 (µMol)1.87600.06071.61058.4440AID1546222
Sodium/glucose cotransporter 2Homo sapiens (human)IC50 (µMol)0.00760.00050.16534.1000AID1396969; AID1413445; AID1546223; AID657588
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Activation Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Sodium/glucose cotransporter 1Homo sapiens (human)EC50 (µMol)1.90000.00111.25448.3000AID1546902
Sodium/glucose cotransporter 2Homo sapiens (human)EC50 (µMol)0.00740.00110.11071.3900AID1546903
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (18)

Processvia Protein(s)Taxonomy
chloride transmembrane transportSodium/glucose cotransporter 1Homo sapiens (human)
glucose transmembrane transportSodium/glucose cotransporter 1Homo sapiens (human)
alpha-glucoside transportSodium/glucose cotransporter 1Homo sapiens (human)
intestinal D-glucose absorptionSodium/glucose cotransporter 1Homo sapiens (human)
response to inorganic substanceSodium/glucose cotransporter 1Homo sapiens (human)
pentose transmembrane transportSodium/glucose cotransporter 1Homo sapiens (human)
fucose transmembrane transportSodium/glucose cotransporter 1Homo sapiens (human)
galactose transmembrane transportSodium/glucose cotransporter 1Homo sapiens (human)
myo-inositol transportSodium/glucose cotransporter 1Homo sapiens (human)
transepithelial water transportSodium/glucose cotransporter 1Homo sapiens (human)
renal glucose absorptionSodium/glucose cotransporter 1Homo sapiens (human)
glucose import across plasma membraneSodium/glucose cotransporter 1Homo sapiens (human)
sodium ion import across plasma membraneSodium/glucose cotransporter 1Homo sapiens (human)
intestinal hexose absorptionSodium/glucose cotransporter 1Homo sapiens (human)
transport across blood-brain barrierSodium/glucose cotransporter 1Homo sapiens (human)
glucose transmembrane transportSodium/glucose cotransporter 1Homo sapiens (human)
sodium ion transportSodium/glucose cotransporter 1Homo sapiens (human)
alpha-glucoside transportSodium/glucose cotransporter 2Homo sapiens (human)
carbohydrate metabolic processSodium/glucose cotransporter 2Homo sapiens (human)
hexose transmembrane transportSodium/glucose cotransporter 2Homo sapiens (human)
renal glucose absorptionSodium/glucose cotransporter 2Homo sapiens (human)
glucose import across plasma membraneSodium/glucose cotransporter 2Homo sapiens (human)
sodium ion import across plasma membraneSodium/glucose cotransporter 2Homo sapiens (human)
sodium ion transportSodium/glucose cotransporter 2Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (12)

Processvia Protein(s)Taxonomy
galactose transmembrane transporter activitySodium/glucose cotransporter 1Homo sapiens (human)
glucose transmembrane transporter activitySodium/glucose cotransporter 1Homo sapiens (human)
myo-inositol:sodium symporter activitySodium/glucose cotransporter 1Homo sapiens (human)
water transmembrane transporter activitySodium/glucose cotransporter 1Homo sapiens (human)
glucose:sodium symporter activitySodium/glucose cotransporter 1Homo sapiens (human)
protein bindingSodium/glucose cotransporter 1Homo sapiens (human)
pentose transmembrane transporter activitySodium/glucose cotransporter 1Homo sapiens (human)
fucose transmembrane transporter activitySodium/glucose cotransporter 1Homo sapiens (human)
alpha-glucoside transmembrane transporter activitySodium/glucose cotransporter 1Homo sapiens (human)
galactose:sodium symporter activitySodium/glucose cotransporter 1Homo sapiens (human)
D-glucose transmembrane transporter activitySodium/glucose cotransporter 1Homo sapiens (human)
low-affinity glucose:sodium symporter activitySodium/glucose cotransporter 2Homo sapiens (human)
glucose:sodium symporter activitySodium/glucose cotransporter 2Homo sapiens (human)
protein bindingSodium/glucose cotransporter 2Homo sapiens (human)
alpha-glucoside transmembrane transporter activitySodium/glucose cotransporter 2Homo sapiens (human)
D-glucose transmembrane transporter activitySodium/glucose cotransporter 2Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (9)

Processvia Protein(s)Taxonomy
early endosomeSodium/glucose cotransporter 1Homo sapiens (human)
plasma membraneSodium/glucose cotransporter 1Homo sapiens (human)
apical plasma membraneSodium/glucose cotransporter 1Homo sapiens (human)
brush border membraneSodium/glucose cotransporter 1Homo sapiens (human)
intracellular organelleSodium/glucose cotransporter 1Homo sapiens (human)
perinuclear region of cytoplasmSodium/glucose cotransporter 1Homo sapiens (human)
extracellular exosomeSodium/glucose cotransporter 1Homo sapiens (human)
intracellular vesicleSodium/glucose cotransporter 1Homo sapiens (human)
plasma membraneSodium/glucose cotransporter 1Homo sapiens (human)
plasma membraneSodium/glucose cotransporter 2Homo sapiens (human)
membraneSodium/glucose cotransporter 2Homo sapiens (human)
apical plasma membraneSodium/glucose cotransporter 2Homo sapiens (human)
extracellular exosomeSodium/glucose cotransporter 2Homo sapiens (human)
plasma membraneSodium/glucose cotransporter 2Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (34)

Assay IDTitleYearJournalArticle
AID657589Selectivity index, ratio of IC50 for human SGLT1 to IC50 for human SGLT22012Bioorganic & medicinal chemistry, May-15, Volume: 20, Issue:10
Discovery of Ipragliflozin (ASP1941): a novel C-glucoside with benzothiophene structure as a potent and selective sodium glucose co-transporter 2 (SGLT2) inhibitor for the treatment of type 2 diabetes mellitus.
AID657599AUC (0 to 24 hrs) in Sprague-Dawley rat at 1 mg/kg, po2012Bioorganic & medicinal chemistry, May-15, Volume: 20, Issue:10
Discovery of Ipragliflozin (ASP1941): a novel C-glucoside with benzothiophene structure as a potent and selective sodium glucose co-transporter 2 (SGLT2) inhibitor for the treatment of type 2 diabetes mellitus.
AID657590Antidiabetic activity in mouse assessed as induction of urinary glucose excretion at 0.01 to 10 mg/kg, po administered as single dose after 24 hrs2012Bioorganic & medicinal chemistry, May-15, Volume: 20, Issue:10
Discovery of Ipragliflozin (ASP1941): a novel C-glucoside with benzothiophene structure as a potent and selective sodium glucose co-transporter 2 (SGLT2) inhibitor for the treatment of type 2 diabetes mellitus.
AID657592Antidiabetic activity in KKAy mouse type 2 diabetic model assessed as decrease in blood glucose level at 0.1 to 1 mg/kg, po administered as single dose after 8 hrs2012Bioorganic & medicinal chemistry, May-15, Volume: 20, Issue:10
Discovery of Ipragliflozin (ASP1941): a novel C-glucoside with benzothiophene structure as a potent and selective sodium glucose co-transporter 2 (SGLT2) inhibitor for the treatment of type 2 diabetes mellitus.
AID657596Tmax in Sprague-Dawley rat at 1 mg/kg, po2012Bioorganic & medicinal chemistry, May-15, Volume: 20, Issue:10
Discovery of Ipragliflozin (ASP1941): a novel C-glucoside with benzothiophene structure as a potent and selective sodium glucose co-transporter 2 (SGLT2) inhibitor for the treatment of type 2 diabetes mellitus.
AID1546225Antidiabetic activity in human T2DM patients assessed as fasting blood glucose level at 50 mg, po for 24 weeks2019European journal of medicinal chemistry, Dec-15, Volume: 184Synthetic strategy and SAR studies of C-glucoside heteroaryls as SGLT2 inhibitor: A review.
AID657601AUC (infinity) in Sprague-Dawley rat at 1 mg/kg, po2012Bioorganic & medicinal chemistry, May-15, Volume: 20, Issue:10
Discovery of Ipragliflozin (ASP1941): a novel C-glucoside with benzothiophene structure as a potent and selective sodium glucose co-transporter 2 (SGLT2) inhibitor for the treatment of type 2 diabetes mellitus.
AID1546223Inhibition of human SGLT22019European journal of medicinal chemistry, Dec-15, Volume: 184Synthetic strategy and SAR studies of C-glucoside heteroaryls as SGLT2 inhibitor: A review.
AID1546902Inhibition of SGLT1 (unknown origin)2020Journal of medicinal chemistry, 05-28, Volume: 63, Issue:10
The Race to Bash NASH: Emerging Targets and Drug Development in a Complex Liver Disease.
AID657598AUC (0 to 24 hrs) in Sprague-Dawley rat at 0.3 mg/kg, iv2012Bioorganic & medicinal chemistry, May-15, Volume: 20, Issue:10
Discovery of Ipragliflozin (ASP1941): a novel C-glucoside with benzothiophene structure as a potent and selective sodium glucose co-transporter 2 (SGLT2) inhibitor for the treatment of type 2 diabetes mellitus.
AID1396969Inhibition of SGLT2 (unknown origin)2018Bioorganic & medicinal chemistry, 08-07, Volume: 26, Issue:14
Design, synthesis and biological evaluation of nitric oxide releasing derivatives of dapagliflozin as potential anti-diabetic and anti-thrombotic agents.
AID657603Oral bioavailability in Sprague-Dawley rat at 1 mg/kg2012Bioorganic & medicinal chemistry, May-15, Volume: 20, Issue:10
Discovery of Ipragliflozin (ASP1941): a novel C-glucoside with benzothiophene structure as a potent and selective sodium glucose co-transporter 2 (SGLT2) inhibitor for the treatment of type 2 diabetes mellitus.
AID657591Antidiabetic activity in KKAy mouse type 2 diabetic model assessed as induction of urinary glucose excretion at 0.01 to 10 mg/kg, po administered as single dose after 24 hrs2012Bioorganic & medicinal chemistry, May-15, Volume: 20, Issue:10
Discovery of Ipragliflozin (ASP1941): a novel C-glucoside with benzothiophene structure as a potent and selective sodium glucose co-transporter 2 (SGLT2) inhibitor for the treatment of type 2 diabetes mellitus.
AID657588Inhibition of human SGLT2 expressed in CHO cells assessed as [14C]AMG accumulation after 2 hrs by scintillation counting2012Bioorganic & medicinal chemistry, May-15, Volume: 20, Issue:10
Discovery of Ipragliflozin (ASP1941): a novel C-glucoside with benzothiophene structure as a potent and selective sodium glucose co-transporter 2 (SGLT2) inhibitor for the treatment of type 2 diabetes mellitus.
AID657597Cmax in Sprague-Dawley rat at 1 mg/kg, po2012Bioorganic & medicinal chemistry, May-15, Volume: 20, Issue:10
Discovery of Ipragliflozin (ASP1941): a novel C-glucoside with benzothiophene structure as a potent and selective sodium glucose co-transporter 2 (SGLT2) inhibitor for the treatment of type 2 diabetes mellitus.
AID657600AUC (infinity) in Sprague-Dawley rat at 0.3 mg/kg, iv2012Bioorganic & medicinal chemistry, May-15, Volume: 20, Issue:10
Discovery of Ipragliflozin (ASP1941): a novel C-glucoside with benzothiophene structure as a potent and selective sodium glucose co-transporter 2 (SGLT2) inhibitor for the treatment of type 2 diabetes mellitus.
AID1546222Inhibition of human SGLT12019European journal of medicinal chemistry, Dec-15, Volume: 184Synthetic strategy and SAR studies of C-glucoside heteroaryls as SGLT2 inhibitor: A review.
AID1546232Selectivity ratio of IC50 for inhibition of human SGLT1 to IC50 for inhibition of human SGLT22019European journal of medicinal chemistry, Dec-15, Volume: 184Synthetic strategy and SAR studies of C-glucoside heteroaryls as SGLT2 inhibitor: A review.
AID1413446Selectivity ratio of IC50 for recombinant human full-length SGLT1 expressed in CHO cells to IC50 for recombinant human full-length SGLT2 expressed in CHO cells2018MedChemComm, Aug-01, Volume: 9, Issue:8
Sodium-glucose cotransporter 2 (SGLT-2) inhibitors: a new antidiabetic drug class.
AID1546224Antidiabetic activity in human T2DM patients assessed as reduction in HbA1c level at 50 mg, po for 24 weeks relative to control2019European journal of medicinal chemistry, Dec-15, Volume: 184Synthetic strategy and SAR studies of C-glucoside heteroaryls as SGLT2 inhibitor: A review.
AID657604Volume of distribution at steady state in Sprague-Dawley rat at 0.3 mg/kg, iv2012Bioorganic & medicinal chemistry, May-15, Volume: 20, Issue:10
Discovery of Ipragliflozin (ASP1941): a novel C-glucoside with benzothiophene structure as a potent and selective sodium glucose co-transporter 2 (SGLT2) inhibitor for the treatment of type 2 diabetes mellitus.
AID1546226Antidiabetic activity in human T2DM patients assessed as reduction in body weight at 50 mg, po for 24 weeks2019European journal of medicinal chemistry, Dec-15, Volume: 184Synthetic strategy and SAR studies of C-glucoside heteroaryls as SGLT2 inhibitor: A review.
AID657593Antidiabetic activity in streptozotocin-induced Sprague-Dawley rat type 1 diabetic model assessed as decrease in blood glucose level at 0.1 to 1 mg/kg, po administered as single dose after 8 hrs2012Bioorganic & medicinal chemistry, May-15, Volume: 20, Issue:10
Discovery of Ipragliflozin (ASP1941): a novel C-glucoside with benzothiophene structure as a potent and selective sodium glucose co-transporter 2 (SGLT2) inhibitor for the treatment of type 2 diabetes mellitus.
AID1413445Inhibition of recombinant human full-length SGLT2 expressed in CHO cells assessed as decrease in [14C]-AMG uptake measured after 2 hrs by topcount scintillation counting method2018MedChemComm, Aug-01, Volume: 9, Issue:8
Sodium-glucose cotransporter 2 (SGLT-2) inhibitors: a new antidiabetic drug class.
AID1546903Inhibition of SGLT2 (unknown origin)2020Journal of medicinal chemistry, 05-28, Volume: 63, Issue:10
The Race to Bash NASH: Emerging Targets and Drug Development in a Complex Liver Disease.
AID657594Half life in Sprague-Dawley rat at 0.3 mg/kg, iv2012Bioorganic & medicinal chemistry, May-15, Volume: 20, Issue:10
Discovery of Ipragliflozin (ASP1941): a novel C-glucoside with benzothiophene structure as a potent and selective sodium glucose co-transporter 2 (SGLT2) inhibitor for the treatment of type 2 diabetes mellitus.
AID657595Half life in Sprague-Dawley rat at 1 mg/kg, po2012Bioorganic & medicinal chemistry, May-15, Volume: 20, Issue:10
Discovery of Ipragliflozin (ASP1941): a novel C-glucoside with benzothiophene structure as a potent and selective sodium glucose co-transporter 2 (SGLT2) inhibitor for the treatment of type 2 diabetes mellitus.
AID657602Total clearance in Sprague-Dawley rat at 0.3 mg/kg, iv2012Bioorganic & medicinal chemistry, May-15, Volume: 20, Issue:10
Discovery of Ipragliflozin (ASP1941): a novel C-glucoside with benzothiophene structure as a potent and selective sodium glucose co-transporter 2 (SGLT2) inhibitor for the treatment of type 2 diabetes mellitus.
AID1346965Human Sodium/glucose cotransporter 2 (Hexose transporter family)2012Naunyn-Schmiedeberg's archives of pharmacology, Apr, Volume: 385, Issue:4
Pharmacological profile of ipragliflozin (ASP1941), a novel selective SGLT2 inhibitor, in vitro and in vivo.
AID1346942Mouse Sodium/glucose cotransporter 1 (Hexose transporter family)2012Naunyn-Schmiedeberg's archives of pharmacology, Apr, Volume: 385, Issue:4
Pharmacological profile of ipragliflozin (ASP1941), a novel selective SGLT2 inhibitor, in vitro and in vivo.
AID1346952Rat Sodium/glucose cotransporter 2 (Hexose transporter family)2012Naunyn-Schmiedeberg's archives of pharmacology, Apr, Volume: 385, Issue:4
Pharmacological profile of ipragliflozin (ASP1941), a novel selective SGLT2 inhibitor, in vitro and in vivo.
AID1346969Mouse Sodium/glucose cotransporter 2 (Hexose transporter family)2012Naunyn-Schmiedeberg's archives of pharmacology, Apr, Volume: 385, Issue:4
Pharmacological profile of ipragliflozin (ASP1941), a novel selective SGLT2 inhibitor, in vitro and in vivo.
AID1346974Rat Sodium/glucose cotransporter 1 (Hexose transporter family)2012Naunyn-Schmiedeberg's archives of pharmacology, Apr, Volume: 385, Issue:4
Pharmacological profile of ipragliflozin (ASP1941), a novel selective SGLT2 inhibitor, in vitro and in vivo.
AID1346950Human Sodium/glucose cotransporter 1 (Hexose transporter family)2012Naunyn-Schmiedeberg's archives of pharmacology, Apr, Volume: 385, Issue:4
Pharmacological profile of ipragliflozin (ASP1941), a novel selective SGLT2 inhibitor, in vitro and in vivo.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (172)

TimeframeStudies, This Drug (%)All Drugs %
pre-19900 (0.00)18.7374
1990's0 (0.00)18.2507
2000's0 (0.00)29.6817
2010's130 (75.58)24.3611
2020's42 (24.42)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 37.55

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 strong demand-to-supply ratio for research on this compound.

MetricThis Compound (vs All)
Research Demand Index37.55 (24.57)
Research Supply Index5.40 (2.92)
Research Growth Index4.57 (4.65)
Search Engine Demand Index54.33 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (37.55)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials45 (25.71%)5.53%
Reviews24 (13.71%)6.00%
Case Studies14 (8.00%)4.05%
Observational7 (4.00%)0.25%
Other85 (48.57%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (56)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
ASP1941 Phase I Study -Placebo-controlled, Single-dose and Repeated-dose Oral Administration Study in Healthy Adult Male Subjects- [NCT01121198]Phase 184 participants (Actual)Interventional2006-12-31Completed
A Double-blind, Placebo-controlled, Dose Escalating Study to Assess the Safety, Tolerability, and Pharmacokinetics of Multiple Oral Doses of ASP1941 and to Explore the Effect of ASP1941 on Urine and Blood Glucose Levels in Healthy Subjects [NCT01288898]Phase 148 participants (Actual)Interventional2007-05-31Completed
A Phase 1, Open-Label, Single-Dose Study to Assess the Effect of Hepatic Function on the Pharmacokinetics and Safety of ASP1941 [NCT01187186]Phase 116 participants (Actual)Interventional2010-05-31Completed
An Open-label, Randomized Crossover Study to Evaluate the Effect of ASP1941 on the Pharmacokinetics, Pharmacodynamics, Safety and Tolerability of Glimepiride in Healthy Subjects and Vice Versa [NCT01302158]Phase 152 participants (Actual)Interventional2009-12-31Completed
An Open Label Study to Evaluate the Pharmacokinetics of ASP1941 After a Single Oral Dose of 14C-labeled ASP1941 in Healthy Male Subjects [NCT01302132]Phase 16 participants (Actual)Interventional2008-05-31Completed
A Phase I Study to Assess Drug-Drug Interaction Between ASP1941 and Miglitol. [NCT01099839]Phase 130 participants (Actual)Interventional2010-02-28Completed
An Open-label, Parallel Group Study to Assess the Effect of Different Grades of Renal Impairment in Patients With Type 2 Diabetes Mellitus on the Pharmacokinetics, Pharmacodynamics and Safety & Tolerability of ASP1941 Relative to Type 2 Diabetes Mellitus [NCT01302028]Phase 140 participants (Actual)Interventional2010-01-22Completed
A Phase 1, Open Label, Randomized, Crossover, Drug Interaction Study of the Pharmacokinetics of ASP1941 and Pioglitazone Hydrochloride After Separate and Concomitant Administration to Healthy Adult Subjects [NCT01088919]Phase 164 participants (Actual)Interventional2009-11-30Completed
Investigation for Clinical Efficacy and Safety of Ipragliflozin 50mg and 100mg on Type II Diabetes [NCT02317484]231 participants (Actual)Observational2014-11-30Completed
Phase 2b, Double-Blind, Randomized, Multicenter, Parallel Group, Placebo-Controlled, Dose-Finding Study to Evaluate the Efficacy, Safety and Tolerability of a 12-Week Treatment With ASP1941 in Combination With Metformin in Patients With Type 2Diabetes Mel [NCT01117584]Phase 2343 participants (Actual)Interventional2010-04-06Completed
A Phase III, Multicenter, Randomized, Placebo-Controlled, Parallel-Group, Double-Blind Trial to Assess the Safety and Efficacy of Addition of Sitagliptin in Japanese Patients With Type 2 Diabetes Mellitus Who Have Inadequate Glycemic Control on Ipragliflo [NCT02577016]Phase 3141 participants (Actual)Interventional2015-11-05Completed
Postmarketing Clinical Study of Ipragliflozin - Long-term Study in Combination With GLP-1 Receptor Agonists in Patients With Type 2 Diabetes Mellitus [NCT02291874]Phase 4100 participants (Actual)Interventional2014-10-08Completed
A Phase 1, Open Label, Randomized, Crossover, Drug Interaction Study of the Pharmacokinetics of ASP1941 and Sitagliptin After Separate and Concomitant Administration to Healthy Adult Subjects [NCT01104532]Phase 164 participants (Actual)Interventional2010-02-28Completed
Postmarketing Clinical Study of Ipragliflozin - Double-blind, Parallel-group Study in Combination With Insulin in Patients With Type 2 Diabetes Mellitus [NCT02175784]Phase 4262 participants (Actual)Interventional2014-03-31Completed
A Phase 2, Double-Blind, Randomized, Placebo and Active-Controlled Dose-Finding Study to Assess the Efficacy, Safety and Tolerability of Multiple Oral Doses of ASP1941 in Patients With Type 2 Diabetes Mellitus [NCT01071850]Phase 2412 participants (Actual)Interventional2010-03-03Completed
An Open-Label Study to Assess the Effect of Different Grades of Renal Impairment in Japanese Patients With Type 2 Diabetes Mellitus on the Pharmacokinetics, Pharmacodynamics, Safety and Tolerability of ASP1941 Relative to Type 2 Diabetes Mellitus Patients [NCT01097681]Phase 125 participants (Actual)Interventional2010-02-16Completed
A Phase 2a, Randomized, Double-Blind, Placebo Controlled, Multiple Dose Study to Assess the Safety and Tolerability of ASP1941 in Adult Subjects With Type 2 Diabetes Mellitus [NCT00790660]Phase 261 participants (Actual)Interventional2008-10-23Completed
A Phase III Study to Assess the Efficacy, Safety and Tolerability of ASP1941 in Combination With Pioglitazone in Patients With Type 2 Diabetes Mellitus Who Have Inadequate Glycemic Control on Pioglitazone Alone [NCT01225081]Phase 3152 participants (Actual)Interventional2010-09-15Completed
Specified Drug Use resulTs survEy of IpragLifLozin treAtment in ELDERly type2 Diabetes Patients (STELLA-ELDER) [NCT02297620]8,687 participants (Actual)Observational2014-04-30Completed
A Phase 1, Randomized, Double-Blind, Placebo- and Active-Controlled Crossover Study to Evaluate the Effect of Repeat Oral Doses of ASP1941 on Cardiac Repolarization in Healthy Male and Female Adult Subjects [NCT01232413]Phase 188 participants (Actual)Interventional2010-09-30Completed
A Double-blind, Randomized, Placebo-controlled Study to Assess the Safety, Tolerability, Pharmacokinetics, and Pharmacodynamics of Single Oral Doses of ASP1941 in Healthy Male Taiwanese Subjects [NCT01373060]Phase 156 participants (Actual)Interventional2011-02-28Completed
A Double-blind, Placebo-controlled, Dose Escalating Study to Assess the Safety, Tolerability, Pharmacokinetics, Pharmacodynamics and Food-effect of Single Oral Doses of ASP1941 in Healthy Male Subjects [NCT01288885]Phase 176 participants (Actual)Interventional2006-11-30Completed
A Phase 2, Clinical Pharmacological Study of ASP1941 in Japanese Patients With Type 1 Diabetes Mellitus [NCT02529449]Phase 243 participants (Actual)Interventional2015-09-01Completed
A Double-blind, Randomized, Placebo-controlled, Parallel Design Study, in Patients With Type 2 Diabetes Mellitus, to Investigate the Safety, Pharmacokinetics and Pharmacodynamics Interactions of Multiple Oral Doses of ASP1941 and Metformin [NCT01302145]Phase 136 participants (Actual)Interventional2009-02-25Completed
A Phase 3 Study to Assess the Efficacy and Safety of ASP1941 in Combination With Metformin in Patients With Type 2 Diabetes Mellitus Who Have Inadequate Glycemic Control on Metformin Alone [NCT01135433]Phase 3168 participants (Actual)Interventional2010-05-15Completed
A Phase 4, Randomized, Open-label, Active-controlled, Multicenter Study to Evaluate the Renal Protective Effect (UACR), Efficacy and Safety of Ipragliflozin in Type 2 Diabetes Mellitus Patients With Albuminuria [NCT03118713]Phase 433 participants (Actual)Interventional2017-04-25Terminated(stopped due to Business decision due to enrollment challenges)
A Phase 1, Randomized, Double-blind, Placebo Controlled, Monotherapy Study to Assess the Pharmacodynamics, Pharmacokinetics, Safety and Tolerability of ASP1941 in Japanese Patients With Type 2 Diabetes Mellitus [NCT01023945]Phase 130 participants (Actual)Interventional2009-11-07Completed
A Phase 3, Double-blind, Randomized Study to Assess the Efficacy and Safety of Ipragliflozin in Combination With Metformin Compared to Metformin Plus Placebo in Subjects in Russia With Type 2 Diabetes Mellitus Who Have Inadequate Glycemic Control on Metfo [NCT02794792]Phase 3268 participants (Actual)Interventional2016-05-11Completed
ASP1941 Phase II Clinical Study - A Double-blind, Placebo-controlled, Parallel-group, Dose-response Study in Patients With Type 2 Diabetes Mellitus [NCT00621868]Phase 2361 participants (Actual)Interventional2008-03-26Completed
Pharmacokinetic Study of ASP1941 -A Pharmacokinetic Study to Assess Drug-Drug Interaction Between ASP1941 and Mitiglinide Calcium Hydrate [NCT01403818]Phase 160 participants (Actual)Interventional2011-06-30Completed
[NCT02791035]Phase 4100 participants (Actual)Interventional2016-06-30Completed
Long-term Study of ASP1941 - A Phase III, Open-Label, Uncontrolled, Monotherapy Study to Assess the Long-term Safety, Tolerability and Efficacy of ASP1941 in Japanese Patients With Type 2 Diabetes Mellitus [NCT01054092]Phase 3182 participants (Actual)Interventional2010-01-14Completed
Phase III Study of ASP1941 -A Phase III, Randomized, Double-Blind, Placebo-controlled, Monotherapy Study to Assess the Efficacy, Safety, and Tolerability of ASP1941 in Japanese Patients With Type 2 Diabetes Mellitus [NCT01057628]Phase 3130 participants (Actual)Interventional2010-01-13Completed
ASP1941 Pharmacokinetic Study - Verification of Bioequivalence Between ASP1941 New Tablets and ASP1941 Conventional Tablets - [NCT01972880]Phase 132 participants (Actual)Interventional2013-09-30Completed
Long-term Study of ASP1941 - Long-term Study in Patients With Type 2 Diabetes Mellitus With Decreased Renal Function (Japanese) [NCT01316094]Phase 3165 participants (Actual)Interventional2011-01-18Completed
[NCT02875821]Phase 444 participants (Actual)Interventional2016-04-26Completed
Post-marketing Clinical Study of Ipragliflozin; Multicenter, Open-label Study to Assess the Efficacy of Ipragliflozin Add-on in Reducing Insulin Dose in Patients With Type 2 Diabetes Mellitus Receiving Insulin Therapy [NCT02847091]Phase 4103 participants (Actual)Interventional2016-07-29Completed
Phase III Study of ASP1941 Double-blind, Parallel-group Study in Combination With Insulin in Patients With Type 1 Diabetes Mellitus [NCT02897219]Phase 3175 participants (Actual)Interventional2016-08-29Completed
Phase III Study of ASP1941 - Open-label, Non-comparative Study to Assess the Long-term Safety, Tolerability and Efficacy of ASP1941 in Combination With an α-Glucosidase Inhibitor in Japanese Patients With Type 2 Diabetes Mellitus Who Have Inadequate Glyce [NCT01242202]Phase 3113 participants (Actual)Interventional2010-10-21Completed
Phase III Study of ASP1941 - Open-label, Non-comparative Study to Assess the Long-term Safety, Tolerability and Efficacy of ASP1941 in Combination With Nateglinide in Japanese Patients With Type 2 Diabetes Mellitus Who Have Inadequate Glycemic Control Wit [NCT01316107]Phase 3122 participants (Actual)Interventional2011-01-15Completed
A Phase III Study to Assess the Efficacy, Safety and Tolerability of ASP1941 in Combination With Sulfonylurea in Patients With Type 2 Diabetes Mellitus Who Have Inadequate Glycemic Control on Sulfonylurea Alone [NCT01242215]Phase 3243 participants (Actual)Interventional2010-09-17Completed
Phase III Study of ASP1941 - Open-label, Non-comparative Study to Assess the Long-term Safety, Tolerability and Efficacy of ASP1941 in Combination With a Dipeptidyl Peptidase-4 Inhibitor in Japanese Patients With Type 2 Diabetes Mellitus Who Have Inadequa [NCT01242228]Phase 3106 participants (Actual)Interventional2010-10-21Completed
A Phase III, Double-Blind, Randomized, Active Controlled, Monotherapy Study to Assess the Efficacy and Safety of ASP1941 in Asian Subjects With Type 2 Diabetes Mellitus [NCT01514838]Phase 346 participants (Actual)Interventional2012-04-23Terminated(stopped due to Discontinued due to company's strategic reason)
Real World Observation of SGLT2 Inhibitors on Clinical Outcomes and Left Ventricular Remodeling in Type 2 Diabetic Patients With Acute Myocardial Infarction, a Prospective, Multi-center Registry Study [NCT05770687]1,000 participants (Anticipated)Observational2020-08-01Recruiting
A Phase 3, Multicenter, Double-Blind, Randomized, Parallel-group, Placebo-Controlled Study to Assess the Efficacy and Safety of ASP1941 in Subjects With Type 2 Diabetes Mellitus Who Have Inadequate Glycemic Control on Metformin and Sitagliptin [NCT02452632]Phase 3143 participants (Actual)Interventional2015-06-22Completed
A Phase III, Double-Blind, Randomized, Placebo-Controlled Study to Assess the Efficacy and Safety of ASP1941 in Combination With Metformin in Asian Subjects With Type 2 Diabetes Mellitus Who Have Inadequate Glycemic Control on Metformin Alone [NCT01505426]Phase 3171 participants (Actual)Interventional2011-11-28Completed
A Phase III, Multicenter, Open-label Long-term Treatment Trial to Assess the Safety and Efficacy of Addition of Ipragliflozin in Japanese Patients With Type 2 Diabetes Mellitus Who Have Inadequate Glycemic Control on Sitagliptin Monotherapy in Addition to [NCT02564211]Phase 377 participants (Actual)Interventional2015-10-26Completed
Efficacy of Ipragliflozin Compared With Sitagliptin in Uncontrolled Type 2 Diabetes With Sulfonylurea and Metformin [NCT03076112]Phase 3170 participants (Actual)Interventional2017-04-25Completed
An Exploratory Study to Investigate the Effects of Ipragliflozin (ASP1941) on Glucose Homeostasis and Urinary Glucose Excretion in Healthy Subjects and Subjects With Type 2 Diabetes Mellitus (T2DM) [NCT01611363]Phase 144 participants (Actual)Interventional2011-10-27Completed
A Clinical Pharmacological Study to Assess Pharmacodynamic and Pharmacokinetic Interactions Between Furosemide and Ipragliflozin in Healthy Subjects [NCT01611415]Phase 124 participants (Actual)Interventional2011-07-31Completed
A Single Dose, Open-label, Randomized Two-period Crossover Study in Healthy Young Subjects to Assess the Absolute Bioavailability of Ipragliflozin [NCT01611428]Phase 114 participants (Actual)Interventional2011-06-30Completed
A Phase III, Multicenter, Randomized, Placebo-Controlled, Parallel-Group, Double-Blind Trial to Assess the Safety and Efficacy of Addition of Ipragliflozin in Japanese Patients With Type 2 Diabetes Mellitus Who Have Inadequate Glycemic Control on Sitaglip [NCT02577003]Phase 3143 participants (Actual)Interventional2015-11-09Completed
Phase III Study of ASP1941 -A Phase III, Open-Label, Uncontrolled, Monotherapy Study to Assess the Long-term Safety, Tolerability and Efficacy of ASP1941 in Japanese Patients With Type 2 Diabetes Mellitus [NCT01672762]Phase 3174 participants (Actual)Interventional2012-05-25Completed
A Pharmacokinetic Study to Investigate the Effect of Food on the Pharmacokinetics of ASP1941 [NCT01674777]Phase 130 participants (Actual)Interventional2010-10-31Completed
A Phase 1, Double-Blind, Placebo-Controlled, Randomized Study to Assess the Pharmacokinetics, Safety and Tolerability of Repeat Oral Dosing of ASP1941 and to Explore the Effect of ASP1941 on Glucose Levels in Healthy Adult Subjects (18 to 45 Years and ≥ 6 [NCT01678287]Phase 165 participants (Actual)Interventional2007-11-30Completed
Specified Drug Use resulTs survEy of lpragLifLozin treAtment in type2 Diabetes Patients: LONG-TERM (STELLA-LONG TERM) [NCT02479399]11,412 participants (Actual)Observational2014-07-17Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT02564211 (3) [back to overview]Change From Baseline in HbA1c
NCT02564211 (3) [back to overview]Percentage of Participants Who Experienced at Least 1 Adverse Event (AE)
NCT02564211 (3) [back to overview]Percentage of Participants Who Had Study Drug Discontinued Due to an AE
NCT02577003 (7) [back to overview]Change From Baseline in 2-hr PMG at Week 24
NCT02577003 (7) [back to overview]Change From Baseline in Body Weight at Week 24
NCT02577003 (7) [back to overview]Change From Baseline in FPG at Week 24
NCT02577003 (7) [back to overview]Change From Baseline in Glucose Total AUC0-2hr After Meal at Week 24
NCT02577003 (7) [back to overview]Change From Baseline in HbA1c at Week 24
NCT02577003 (7) [back to overview]Percentage of Participants Who Discontinued Study Drug Due to an AE
NCT02577003 (7) [back to overview]Percentage of Participants Who Experienced at Least One Adverse Event (AE)
NCT02577016 (6) [back to overview]Change From Baseline in 2-hr PMG at Week 24
NCT02577016 (6) [back to overview]Change From Baseline in FPG at Week 24
NCT02577016 (6) [back to overview]Change From Baseline in Glucose Total Area Under the Plasma Concentration Curve From Hour 0 to Hour 2 (AUC0-2hr) After Meal at Week 24
NCT02577016 (6) [back to overview]Change From Baseline in HbA1c at Week 24
NCT02577016 (6) [back to overview]Percentage of Participants Who Discontinued Study Drug Due to an AE
NCT02577016 (6) [back to overview]Percentage of Participants Who Experienced at Least One Adverse Event (AE)

Change From Baseline in HbA1c

Participants had HbA1c levels determined at baseline and at Week 52. HbA1c is reported as a percentage. A negative number reflects a decrease in percentage. (NCT02564211)
Timeframe: Baseline and Week 52

InterventionPercent (Mean)
Ipragliflozin-0.80

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Percentage of Participants Who Experienced at Least 1 Adverse Event (AE)

An AE was any unfavorable or unintended sign, symptom, or disease, and a causal relationship to the relevant investigational product is not considered. An AE could therefore be any unfavorable and unintended sign, including results from laboratory assessments, physical examination, electrocardiograms, and vital sign assessments. The percentage of participants that had AE was recorded. (NCT02564211)
Timeframe: Up to 54 weeks

InterventionPercentage of participants (Number)
Ipragliflozin77.9

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Percentage of Participants Who Had Study Drug Discontinued Due to an AE

The percentage of participants who had study treatment stopped due to an AE regardless if they completed study. (NCT02564211)
Timeframe: Up to 52 weeks

InterventionPercentage of Participants (Number)
Ipragliflozin5.2

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Change From Baseline in 2-hr PMG at Week 24

Change from baseline in 2-hr PMG at Week 24 is defined as Week 24 2-hr PMG minus Week 0 2-hr PMG. Statistical analysis based on a cLDA model with terms for treatment, time, prior use of AHAs, the interactions of treatment by time, time by prior use of AHAs, treatment by time by prior use of AHAs, and baseline eGFR value with the constraint that the mean baseline 2-hr PMG is the same for both treatment groups. (NCT02577003)
Timeframe: Baseline and Week 24

Interventionmg/dL (Least Squares Mean)
Ipragliflozin + Sitagliptin-52.4
Placebo + Sitagliptin-3.8

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Change From Baseline in Body Weight at Week 24

Change from baseline in body weight at Week 24 is defined as Week 24 body weight minus Week 0 body weight. Statistical analysis based on a cLDA model with terms for treatment, time, prior use of AHAs, the interactions of treatment by time, time by prior use of AHAs and treatment by time by prior use of AHAs, and baseline eGFR value with the constraint that the mean baseline body weight is the same for both treatment groups. (NCT02577003)
Timeframe: Baseline and Week 24

Interventionkg (Least Squares Mean)
Ipragliflozin + Sitagliptin-2.4
Placebo + Sitagliptin-0.6

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Change From Baseline in FPG at Week 24

Change from baseline in FPG at Week 24 is defined as Week 24 FPG minus Week 0 FPG. Statistical analysis based on a cLDA model with terms for treatment, time, prior use of AHAs, the interactions of treatment by time, time by prior use of AHAs, treatment by time by prior use of AHAs, and baseline eGFR value with the constraint that the mean baseline FPG is the same for both treatment groups. (NCT02577003)
Timeframe: Baseline and Week 24

Interventionmg/dL (Least Squares Mean)
Ipragliflozin + Sitagliptin-30.3
Placebo + Sitagliptin-2.1

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Change From Baseline in Glucose Total AUC0-2hr After Meal at Week 24

Change from baseline in glucose total AUC0-2hr after meal at Week 24 is defined as Week 24 glucose total AUC0-2hr after a meal minus Week 0 glucose total AUC0-2hr after a meal. Statistical analysis based on a cLDA model with terms for treatment, time, prior use of AHAs, the interactions of treatment by time, time by prior use of AHAs and treatment by time by prior use of AHAs, and baseline eGFR value with the constraint that the mean baseline glucose total AUC0-2hr after meal is the same for both treatment groups. (NCT02577003)
Timeframe: Baseline and Week 24 (just before the loading meal [0 min], 30 min, 60 min and 120 min)

Interventionmg･hr/dL (Least Squares Mean)
Ipragliflozin + Sitagliptin-86.9
Placebo + Sitagliptin-2.3

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Change From Baseline in HbA1c at Week 24

HbA1c is measured as percent. Thus, this change from baseline reflects the Week 24 HbA1c percent minus the Week 0 HbA1c percent. Statistical analysis based on a constrained longitudinal data analysis (cLDA) model with terms for treatment, time, prior use of AHAs, the interactions of treatment by time, time by prior use of AHAs, treatment by time by prior use of AHAs, and baseline eGFR value with the constraint that the mean baseline HbA1c is the same for both treatment groups. (NCT02577003)
Timeframe: Baseline and Week 24

InterventionPercent (Least Squares Mean)
Ipragliflozin + Sitagliptin-0.84
Placebo + Sitagliptin-0.07

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Percentage of Participants Who Discontinued Study Drug Due to an AE

An adverse event is defined as any untoward medical occurrence in a participant or clinical investigation participant administered a pharmaceutical product and which does not necessarily have to have a causal relationship with this treatment. (NCT02577003)
Timeframe: Up to 24 weeks

InterventionPercentage of participants (Number)
Ipragliflozin + Sitagliptin2.7
Placebo + Sitagliptin5.7

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Percentage of Participants Who Experienced at Least One Adverse Event (AE)

An adverse event is defined as any untoward medical occurrence in a participant or clinical investigation participant administered a pharmaceutical product and which does not necessarily have to have a causal relationship with this treatment. (NCT02577003)
Timeframe: Up to 26 weeks

InterventionPercentage of participants (Number)
Ipragliflozin + Sitagliptin50.7
Placebo + Sitagliptin65.7

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Change From Baseline in 2-hr PMG at Week 24

Change from baseline in 2-hr PMG at Week 24 is defined as Week 24 2-hr PMG minus Week 0 2-hr PMG. Statistical analysis based on a cLDA model with terms for treatment, time, prior use of AHAs, the interactions of treatment by time, time by prior use of AHAs, and treatment by time by prior use of AHAs with the constraint that the mean baseline 2-hr PMG is the same for both treatment groups. (NCT02577016)
Timeframe: Baseline and Week 24

Interventionmg/dL (Least Squares Mean)
Sitagliptin + Ipragliflozin-39.0
Placebo + Ipragliflozin3.4

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Change From Baseline in FPG at Week 24

Change from baseline in FPG at Week 24 is defined as Week 24 FPG minus Week 0 FPG. Statistical analysis based on a cLDA model with terms for treatment, time, prior use of AHAs, the interactions of treatment by time, time by prior use of AHAs, and treatment by time by prior use of AHAs with the constraint that the mean baseline FPG is the same for both treatment groups. (NCT02577016)
Timeframe: Baseline and Week 24

Interventionmg/dL (Least Squares Mean)
Sitagliptin + Ipragliflozin-11.8
Placebo + Ipragliflozin-0.6

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Change From Baseline in Glucose Total Area Under the Plasma Concentration Curve From Hour 0 to Hour 2 (AUC0-2hr) After Meal at Week 24

Change from Baseline in Glucose Total AUC0-2hr after Meal at Week 24 is defined as Week 24 Glucose Total AUC0-2hr after a meal minus Week 0 Glucose Total AUC0-2hr after a meal. Statistical analysis based on a cLDA model with terms for treatment, time, prior use of AHAs, the interactions of treatment by time, time by prior use of AHAs, and treatment by time by prior use of AHAs with the constraint that the mean baseline glucose total AUC0-2hr after meal is the same for both treatment groups. (NCT02577016)
Timeframe: Baseline and Week 24 (just before loading meal [0 min], 30 min, 60 min and 120 min)

Interventionmg･hr/dL (Least Squares Mean)
Sitagliptin + Ipragliflozin-65.7
Placebo + Ipragliflozin1.3

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Change From Baseline in HbA1c at Week 24

HbA1c is measured as percent. Thus, this change from baseline reflects the Week 24 HbA1c percent minus the Week 0 HbA1c percent. Statistical analysis based on a constrained longitudinal data analysis (cLDA) model with terms for treatment, time, prior use of AHAs, the interactions of treatment by time, time by prior use of AHAs, and treatment by time by prior use of AHAs with the constraint that the mean baseline is the same for both treatment groups. (NCT02577016)
Timeframe: Baseline and Week 24

InterventionPercent (Least Squares Mean)
Sitagliptin + Ipragliflozin-0.69
Placebo + Ipragliflozin0.14

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Percentage of Participants Who Discontinued Study Drug Due to an AE

An adverse event is defined as any untoward medical occurrence in a participant or clinical investigation participant administered a pharmaceutical product and which does not necessarily have to have a causal relationship with this treatment. (NCT02577016)
Timeframe: Up to 24 weeks

InterventionPercentage of participants (Number)
Sitagliptin + Ipragliflozin2.9
Placebo + Ipragliflozin0.0

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Percentage of Participants Who Experienced at Least One Adverse Event (AE)

An adverse event is defined as any untoward medical occurrence in a participant or clinical investigation participant administered a pharmaceutical product and which does not necessarily have to have a causal relationship with this treatment. (NCT02577016)
Timeframe: Up to 26 weeks

InterventionPercentage of participants (Number)
Sitagliptin + Ipragliflozin54.3
Placebo + Ipragliflozin63.4

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SubstanceRelationship StrengthStudiesTrialsClassesRoles
chlorine
chloride : A halide anion formed when chlorine picks up an electron to form an an anion.		2.2110halide anion;
monoatomic chlorine		cofactor;
Escherichia coli metabolite;
human metabolite
niacinamide
nicotinamide : A pyridinecarboxamide that is pyridine in which the hydrogen at position 3 is replaced by a carboxamide group.		2.520pyridine alkaloid;
pyridinecarboxamide;
vitamin B3		anti-inflammatory agent;
antioxidant;
cofactor;
EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor;
EC 3.5.1.98 (histone deacetylase) inhibitor;
Escherichia coli metabolite;
geroprotector;
human urinary metabolite;
metabolite;
mouse metabolite;
neuroprotective agent;
Saccharomyces cerevisiae metabolite;
Sir2 inhibitor
uracil
2,4-dihydroxypyrimidine: a urinary biomarker for bipolar disorder		3.5111pyrimidine nucleobase;
pyrimidone		allergen;
Daphnia magna metabolite;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
prodrug;
Saccharomyces cerevisiae metabolite
uric acid
Uric Acid: An oxidation product, via XANTHINE OXIDASE, of oxypurines such as XANTHINE and HYPOXANTHINE. It is the final oxidation product of purine catabolism in humans and primates, whereas in most other mammals URATE OXIDASE further oxidizes it to ALLANTOIN.. uric acid : An oxopurine that is the final oxidation product of purine metabolism.. 6-hydroxy-1H-purine-2,8(7H,9H)-dione : A tautomer of uric acid having oxo groups at C-2 and C-8 and a hydroxy group at C-6.. 7,9-dihydro-1H-purine-2,6,8(3H)-trione : An oxopurine in which the purine ring is substituted by oxo groups at positions 2, 6, and 8.		10.3631uric acidEscherichia coli metabolite;
human metabolite;
mouse metabolite
candesartan
candesartan: a nonpeptide angiotensin II receptor antagonist. candesartan : A benzimidazolecarboxylic acid that is 1H-benzimidazole-7-carboxylic acid substituted by an ethoxy group at position 2 and a ({2'-(1H-tetrazol-5-yl)[1,1'-biphenyl]-4-yl}methyl) group at position 1. It is a angiotensin receptor antagonist used for the treatment of hypertension.		7.110benzimidazolecarboxylic acid;
biphenylyltetrazole		angiotensin receptor antagonist;
antihypertensive agent;
environmental contaminant;
xenobiotic
fenofibrate
Pharmavit: a polyvitamin product, comprising vitamins A, D2, B1, B2, B6, C, E, nicotinamide, & calcium pantothene; may be a promising agent for application to human populations exposed to carcinogenic and genetic hazards of ionizing radiation; RN from CHEMLINE		3.3510aromatic ether;
chlorobenzophenone;
isopropyl ester;
monochlorobenzenes		antilipemic drug;
environmental contaminant;
geroprotector;
xenobiotic
glimepiride
glimepiride: structure given in first source		9.3711sulfonamide
losartan
Losartan: An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.. losartan : A biphenylyltetrazole where a 1,1'-biphenyl group is attached at the 5-position and has an additional trisubstituted imidazol-1-ylmethyl group at the 4'-position		2.1710biphenylyltetrazole;
imidazoles		angiotensin receptor antagonist;
anti-arrhythmia drug;
antihypertensive agent;
endothelin receptor antagonist
metformin
Metformin: A biguanide hypoglycemic agent used in the treatment of non-insulin-dependent diabetes mellitus not responding to dietary modification. Metformin improves glycemic control by improving insulin sensitivity and decreasing intestinal absorption of glucose. (From Martindale, The Extra Pharmacopoeia, 30th ed, p289). metformin : A member of the class of guanidines that is biguanide the carrying two methyl substituents at position 1.		12.382116guanidinesenvironmental contaminant;
geroprotector;
hypoglycemic agent;
xenobiotic
nifedipine
Nifedipine: A potent vasodilator agent with calcium antagonistic action. It is a useful anti-anginal agent that also lowers blood pressure.		7.110C-nitro compound;
dihydropyridine;
methyl ester		calcium channel blocker;
human metabolite;
tocolytic agent;
vasodilator agent
pioglitazone
Pioglitazone: A thiazolidinedione and PPAR GAMMA agonist that is used in the treatment of TYPE 2 DIABETES MELLITUS.. pioglitazone : A member of the class of thiazolidenediones that is 1,3-thiazolidine-2,4-dione substituted by a benzyl group at position 5 which in turn is substituted by a 2-(5-ethylpyridin-2-yl)ethoxy group at position 4 of the phenyl ring. It exhibits hypoglycemic activity.		7.8673aromatic ether;
pyridines;
thiazolidinediones		antidepressant;
cardioprotective agent;
EC 2.7.1.33 (pantothenate kinase) inhibitor;
EC 6.2.1.3 (long-chain-fatty-acid--CoA ligase) inhibitor;
ferroptosis inhibitor;
geroprotector;
hypoglycemic agent;
insulin-sensitizing drug;
PPARgamma agonist;
xenobiotic
sorbitol
D-glucitol : The D-enantiomer of glucitol (also known as D-sorbitol).		3.9430glucitolcathartic;
Escherichia coli metabolite;
food humectant;
human metabolite;
laxative;
metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite;
sweetening agent
hydroxyproline
Hydroxyproline: A hydroxylated form of the imino acid proline. A deficiency in ASCORBIC ACID can result in impaired hydroxyproline formation.. hydroxyproline : A proline derivative that is proline substituted by at least one hydroxy group.		2.11104-hydroxyproline;
L-alpha-amino acid zwitterion		human metabolite;
mouse metabolite;
plant metabolite
phlorhizin
[no description available]		5.7650aryl beta-D-glucoside;
dihydrochalcones;
monosaccharide derivative		antioxidant;
plant metabolite
thiophenes
Thiophenes: A monocyclic heteroarene furan in which the oxygen atom is replaced by a sulfur.. thiophenes : Compounds containing at least one thiophene ring.		18.9416743mancude organic heteromonocyclic parent;
monocyclic heteroarene;
thiophenes;
volatile organic compound		non-polar solvent
pyrazines
Pyrazines: A heterocyclic aromatic organic compound with the chemical formula C4H4N2.. pyrazine : A diazine that is benzene in which the carbon atoms at positions 1 and 4 have been replaced by nitrogen atoms.		4.3711diazine;
pyrazines		Daphnia magna metabolite
chenodeoxycholic acid
Chenodeoxycholic Acid: A bile acid, usually conjugated with either glycine or taurine. It acts as a detergent to solubilize fats for intestinal absorption and is reabsorbed by the small intestine. It is used as cholagogue, a choleretic laxative, and to prevent or dissolve gallstones.. chenodeoxycholic acid : A dihydroxy-5beta-cholanic acid that is (5beta)-cholan-24-oic acid substituted by hydroxy groups at positions 3 and 7 respectively.. chenodeoxycholate : Conjugate base of chenodeoxycholic acid; major species at pH 7.3.		3.3510bile acid;
C24-steroid;
dihydroxy-5beta-cholanic acid		human metabolite;
mouse metabolite
thiazolidines
Thiazolidines: Reduced (protonated) form of THIAZOLES. They can be oxidized to THIAZOLIDINEDIONES.		4.5422thiazolidine
fructosamine
Fructosamine: An amino sugar formed when glucose non-enzymatically reacts with the N-terminal amino group of proteins. The fructose moiety is derived from glucose by the classical Amadori rearrangement.		3.4511
fludrocortisone
Fludrocortisone: A synthetic mineralocorticoid with anti-inflammatory activity.		2.131011beta-hydroxy steroid;
17alpha-hydroxy steroid;
20-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(4) steroid;
C21-steroid;
fluorinated steroid;
mineralocorticoid		adrenergic agent;
anti-inflammatory drug
glucose, (beta-d)-isomer
beta-D-glucose : D-Glucopyranose with beta configuration at the anomeric centre.. (1->4)-beta-D-glucan : A beta-D-glucan in which the glucose units are connected by (1->4) linkages.. (1->3)-beta-D-glucan : A beta-D-glucan in which the glucose units are connected by (1->3) linkages.		18.9716844D-glucopyranoseepitope;
mouse metabolite
fenofibric acid
fenofibric acid: RN given refers to parent cpd without isomeric designation; structure. fenofibric acid : A monocarboxylic acid that is 2-methylpropanoic acid substituted by a 4-(4-chlorobenzoyl)phenoxy group at position 2. It is a metabolite of the drug fenofibrate.		3.3510aromatic ketone;
chlorobenzophenone;
monocarboxylic acid		drug metabolite;
marine xenobiotic metabolite
triazoles
Triazoles: Heterocyclic compounds containing a five-membered ring with two carbon atoms and three nitrogen atoms with the molecular formula C2H3N3.. triazoles : An azole in which the five-membered heterocyclic aromatic skeleton contains three N atoms and two C atoms.		4.37111,2,3-triazole
rosiglitazone
[no description available]		3.3510aminopyridine;
thiazolidinediones		EC 6.2.1.3 (long-chain-fatty-acid--CoA ligase) inhibitor;
ferroptosis inhibitor;
insulin-sensitizing drug
febuxostat
Febuxostat: A thiazole derivative and inhibitor of XANTHINE OXIDASE that is used for the treatment of HYPERURICEMIA in patients with chronic GOUT.. febuxostat : A 1,3-thiazolemonocarboxylic acid that is 4-methyl-1,3-thiazole-5-carboxylic acid which is substituted by a 3-cyano-4-(2-methylpropoxy)phenyl group at position 2. It is an orally-active, potent, and selective xanthine oxidase inhibitor used for the treatment of chronic hyperuricaemia in patients with gout.		3.27101,3-thiazolemonocarboxylic acid;
aromatic ether;
nitrile		EC 1.17.3.2 (xanthine oxidase) inhibitor
moxifloxacin
Moxifloxacin: A fluoroquinolone that acts as an inhibitor of DNA TOPOISOMERASE II and is used as a broad-spectrum antibacterial agent.. moxifloxacin : A quinolone that consists of 4-oxo-1,4-dihydroquinoline-3-carboxylic acid bearing a cyclopropyl substituent at position 1, a fluoro substitiuent at position 6, a (4aS,7aS)-octahydro-6H-pyrrolo[3,4-b]pyridin-6-yl group at position 7 and a methoxy substituent at position 8. A member of the fluoroquinolone class of antibacterial agents.		4.3911aromatic ether;
cyclopropanes;
fluoroquinolone antibiotic;
pyrrolidinopiperidine;
quinolinemonocarboxylic acid;
quinolone antibiotic;
quinolone		antibacterial drug
tak 779
[no description available]		3.3510
glycogen
glycogen : A polydisperse, highly branched glucan composed of chains of D-glucopyranose residues in alpha(1->4) glycosidic linkage, joined together by alpha(1->6) glycosidic linkages. A small number of alpha(1->3) glycosidic linkages and some cumulative alpha(1->6) links also may occur. The branches in glycogen typically contain 8 to 12 glucose residues.		2.1310
obeticholic acid
obeticholic acid: A farnesoid X receptor agonist and anticholestatic agent that is used in the treatment of chronic liver diseases; structure in first source.. obeticholic acid : A dihydroxy-5beta-cholanic acid that is chenodeoxycholic acid carrying an additional ethyl substituent at the 6alpha-position. A semi-synthetic bile acid which acts as a farnesoid X receptor agonist and is used for treatment of primary biliary cholangitis.		3.35103alpha-hydroxy steroid;
7alpha-hydroxy steroid;
dihydroxy-5beta-cholanic acid		farnesoid X receptor agonist;
hepatoprotective agent
glycosides
[no description available]		4.520
topiroxostat
FYX-051: xanthine oxidoreductase inhibitor		3.2710
gft505
[no description available]		3.3510
dapagliflozin
[no description available]		10.97201aromatic ether;
C-glycosyl compound;
monochlorobenzenes		hypoglycemic agent;
sodium-glucose transport protein subtype 2 inhibitor
gw 4064
[no description available]		3.3510stilbenoid
mbx-8025
seladelpar: PPAR-delta agonist		3.3510
cenicriviroc
cenicriviroc: an inhibitor of HIV-1. cenicriviroc : A member of the class of benzazocines that is (5Z)-1,2,3,4-tetrahydro-1-benzazocine which is substituted by a 2-methylpropyl, N-{4-[(S)-(1-propyl-1H-imidazol-5-yl)methanesulfinyl]phenyl}carboxamide and 4-(2-butoxyethoxy)phenyl groups at positions 1, 5 and 8, respectively. It is a potent chemokine 2 and 5 receptor antagonist currently in development for the treatment of liver fibrosis in adults with nonalcoholic steatohepatitis (NASH).		3.3510aromatic ether;
benzazocine;
diether;
imidazoles;
secondary carboxamide;
sulfoxide		anti-HIV agent;
anti-inflammatory agent;
antirheumatic drug;
chemokine receptor 2 antagonist;
chemokine receptor 5 antagonist
alogliptin
alogliptin: structure in first source. alogliptin : A piperidine that is 3-methyl-2,4-dioxo-3,4-dihydropyrimidine carrying additional 2-cyanobenzyl and 3-aminopiperidin-1-yl groups at positions 1 and 2 respectively (the R-enantiomer). Used in the form of its benzoate salt for treatment of type 2 diabetes.		3.5111nitrile;
piperidines;
primary amino compound;
pyrimidines		EC 3.4.14.5 (dipeptidyl-peptidase IV) inhibitor;
hypoglycemic agent
sitagliptin phosphate
Sitagliptin Phosphate: A pyrazine-derived DIPEPTIDYL-PEPTIDASE IV INHIBITOR and HYPOGLYCEMIC AGENT that increases the levels of the INCRETIN hormones GLUCAGON-LIKE PEPTIDE-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). It is used in the treatment of TYPE 2 DIABETES.		9.591211
gw 2580
5-(3-methoxy-4-((4-methoxybenzyl)oxy)benzyl)pyrimidine-2,4-diamine: a cFMS kinase inhibitor; structure in first source		2.1710
empagliflozin
[no description available]		9.51170aromatic ether;
C-glycosyl compound;
monochlorobenzenes;
tetrahydrofuryl ether		hypoglycemic agent;
sodium-glucose transport protein subtype 2 inhibitor
pituitrin
Pituitrin: A substance or extract from the neurohypophysis (PITUITARY GLAND, POSTERIOR).		2.2510
1,5-anhydro-1-(5-(4-ethoxybenzyl)-2-methoxy-4-methylphenyl)-1-thioglucitol
[no description available]		4.5130diarylmethane
glucagon
Glucagon: A 29-amino acid pancreatic peptide derived from proglucagon which is also the precursor of intestinal GLUCAGON-LIKE PEPTIDES. Glucagon is secreted by PANCREATIC ALPHA CELLS and plays an important role in regulation of BLOOD GLUCOSE concentration, ketone metabolism, and several other biochemical and physiological processes. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p1511). glucagon : A 29-amino acid peptide hormone consisting of His, Ser, Gln, Gly, Thr, Phe, Thr, Ser, Asp, Tyr, Ser, Lys, Tyr, Leu, Asp, Ser, Arg, Arg, Ala, Gln, Asp, Phe, Val, Gln, Trp, Leu, Met, Asn and Thr residues joined in sequence.		3.811peptide hormone
liraglutide
[no description available]		2.3110lipopeptide;
polypeptide		glucagon-like peptide-1 receptor agonist;
neuroprotective agent
glucagon-like peptide 1
Glucagon-Like Peptide 1: A peptide of 36 or 37 amino acids that is derived from PROGLUCAGON and mainly produced by the INTESTINAL L CELLS. GLP-1(1-37 or 1-36) is further N-terminally truncated resulting in GLP-1(7-37) or GLP-1-(7-36) which can be amidated. These GLP-1 peptides are known to enhance glucose-dependent INSULIN release, suppress GLUCAGON release and gastric emptying, lower BLOOD GLUCOSE, and reduce food intake.		4.9221
incretins
Incretins: Peptides which stimulate INSULIN release from the PANCREATIC BETA CELLS following oral nutrient ingestion, or postprandially.		3.0410
c-peptide
C-Peptide: The middle segment of proinsulin that is between the N-terminal B-chain and the C-terminal A-chain. It is a pancreatic peptide of about 31 residues, depending on the species. Upon proteolytic cleavage of proinsulin, equimolar INSULIN and C-peptide are released. C-peptide immunoassay has been used to assess pancreatic beta cell function in diabetic patients with circulating insulin antibodies or exogenous insulin. Half-life of C-peptide is 30 min, almost 8 times that of insulin.		10.1433
canagliflozin
canagliflozin hydrate : A hydrate that is the hemihydrate form of canagliflozin. Used for treatment of type II diabetes via inhibition of sodium-glucose transport protein subtype 2.		15.98201C-glycosyl compound;
organofluorine compound;
thiophenes		hypoglycemic agent;
sodium-glucose transport protein subtype 2 inhibitor
azd7687
AZD7687: structure in first source		3.3510
glycolipids
[no description available]		2.1710
piperidines
Piperidines: A family of hexahydropyridines.		3.5111
pf 04971729
ertugliflozin: structure in first source		4.220diarylmethane
deberza
[no description available]		3.69202-benzofurans
natriuretic peptide, brain
Natriuretic Peptide, Brain: A PEPTIDE that is secreted by the BRAIN and the HEART ATRIA, stored mainly in cardiac ventricular MYOCARDIUM. It can cause NATRIURESIS; DIURESIS; VASODILATION; and inhibits secretion of RENIN and ALDOSTERONE. It improves heart function. It contains 32 AMINO ACIDS.		4.0721polypeptide
a 769662
[no description available]		3.3510biphenyls
4-(2-(2-chloro-4-((5-cyclopropyl-3-(2,6-dichlorophenyl)-4-isoxazolyl)methoxy)phenyl)cyclopropyl)benzoic acid
4-(2-(2-chloro-4-((5-cyclopropyl-3-(2,6-dichlorophenyl)-4-isoxazolyl)methoxy)phenyl)cyclopropyl)benzoic acid: a farnesoid X receptor agonist; structure in first source		3.3510
insulin glargine
Insulin Glargine: A recombinant LONG ACTING INSULIN and HYPOGLYCEMIC AGENT that is used to manage BLOOD GLUCOSE in patients with DIABETES MELLITUS.		8.5311
allopurinol
Allopurinol: A XANTHINE OXIDASE inhibitor that decreases URIC ACID production. It also acts as an antimetabolite on some simpler organisms.. allopurinol : A bicyclic structure comprising a pyrazole ring fused to a hydroxy-substituted pyrimidine ring.		3.2710nucleobase analogue;
organic heterobicyclic compound		antimetabolite;
EC 1.17.3.2 (xanthine oxidase) inhibitor;
gout suppressant;
radical scavenger
leptin
Leptin: A 16-kDa peptide hormone secreted from WHITE ADIPOCYTES. Leptin serves as a feedback signal from fat cells to the CENTRAL NERVOUS SYSTEM in regulation of food intake, energy balance, and fat storage.		2.8930
ConditionIndicatedRelationship StrengthStudiesTrials
Alloxan Diabetes
[description not available]		04.51200
Autoimmune Diabetes
[description not available]		09.25147
Diabetes Mellitus, Adult-Onset
[description not available]		018.7813849
Diabetes Mellitus, Type 1
A subtype of DIABETES MELLITUS that is characterized by INSULIN deficiency. It is manifested by the sudden onset of severe HYPERGLYCEMIA, rapid progression to DIABETIC KETOACIDOSIS, and DEATH unless treated with insulin. The disease may occur at any age, but is most common in childhood or adolescence.		111.25147
Diabetes Mellitus, Type 2
A subclass of DIABETES MELLITUS that is not INSULIN-responsive or dependent (NIDDM). It is characterized initially by INSULIN RESISTANCE and HYPERINSULINEMIA; and eventually by GLUCOSE INTOLERANCE; HYPERGLYCEMIA; and overt diabetes. Type II diabetes mellitus is no longer considered a disease exclusively found in adults. Patients seldom develop KETOSIS but often exhibit OBESITY.		120.7813849
Disease Models, Animal
Naturally-occurring or experimentally-induced animal diseases with pathological processes analogous to human diseases.		03.98110
Deep Vein Thrombosis
[description not available]		02.1710
Venous Thrombosis
The formation or presence of a blood clot (THROMBUS) within a vein.		02.1710
Cardiometabolic Syndrome
A cluster of symptoms that are risk factors for CARDIOVASCULAR DISEASES and TYPE 2 DIABETES MELLITUS. The major components not only include metabolic dysfunctions of METABOLIC SYNDROME but also HYPERTENSION, and ABDOMINAL OBESITY.		03.1710
Fatty Liver, Nonalcoholic
[description not available]		08.12162
Obesity
A status with BODY WEIGHT that is grossly above the recommended standards, usually due to accumulation of excess FATS in the body. The standards may vary with age, sex, genetic or cultural background. In the BODY MASS INDEX, a BMI greater than 30.0 kg/m2 is considered obese, and a BMI greater than 40.0 kg/m2 is considered morbidly obese (MORBID OBESITY).		08.24240
Metabolic Syndrome
A cluster of symptoms that are risk factors for CARDIOVASCULAR DISEASES and TYPE 2 DIABETES MELLITUS. The major components of metabolic syndrome include ABDOMINAL OBESITY; atherogenic DYSLIPIDEMIA; HYPERTENSION; HYPERGLYCEMIA; INSULIN RESISTANCE; a proinflammatory state; and a prothrombotic (THROMBOSIS) state.		03.1710
Non-alcoholic Fatty Liver Disease
Fatty liver finding without excessive ALCOHOL CONSUMPTION.		08.12162
Insulin Sensitivity
[description not available]		010.1222
Insulin Resistance
Diminished effectiveness of INSULIN in lowering blood sugar levels: requiring the use of 200 units or more of insulin per day to prevent HYPERGLYCEMIA or KETOSIS.		010.1222
Cirrhosis, Liver
[description not available]		03.7730
Liver Cirrhosis
Liver disease in which the normal microcirculation, the gross vascular anatomy, and the hepatic architecture have been variably destroyed and altered with fibrous septa surrounding regenerated or regenerating parenchymal nodules.		03.7730
Cardiac Failure
[description not available]		04.6651
Heart Failure
A heterogeneous condition in which the heart is unable to pump out sufficient blood to meet the metabolic need of the body. Heart failure can be caused by structural defects, functional abnormalities (VENTRICULAR DYSFUNCTION), or a sudden overload beyond its capacity. Chronic heart failure is more common than acute heart failure which results from sudden insult to cardiac function, such as MYOCARDIAL INFARCTION.		04.6651
Diabetes Mellitus
A heterogeneous group of disorders characterized by HYPERGLYCEMIA and GLUCOSE INTOLERANCE.		17.0880
Liver Steatosis
[description not available]		08.11131
Fatty Liver
Lipid infiltration of the hepatic parenchymal cells resulting in a yellow-colored liver. The abnormal lipid accumulation is usually in the form of TRIGLYCERIDES, either as a single large droplet or multiple small droplets. Fatty liver is caused by an imbalance in the metabolism of FATTY ACIDS.		013.11131
Chronic Kidney Diseases
[description not available]		07.8272
Renal Insufficiency, Chronic
Conditions in which the KIDNEYS perform below the normal level for more than three months. Chronic kidney insufficiency is classified by five stages according to the decline in GLOMERULAR FILTRATION RATE and the degree of kidney damage (as measured by the level of PROTEINURIA). The most severe form is the end-stage renal disease (CHRONIC KIDNEY FAILURE). (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002)		07.8272
Body Weight
The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.		011.94288
Diabetic Glomerulosclerosis
[description not available]		05.0881
Diabetic Nephropathies
KIDNEY injuries associated with diabetes mellitus and affecting KIDNEY GLOMERULUS; ARTERIOLES; KIDNEY TUBULES; and the interstitium. Clinical signs include persistent PROTEINURIA, from microalbuminuria progressing to ALBUMINURIA of greater than 300 mg/24 h, leading to reduced GLOMERULAR FILTRATION RATE and END-STAGE RENAL DISEASE.		05.0881
Breast Cancer
[description not available]		07.2510
Breast Neoplasms
Tumors or cancer of the human BREAST.		02.2510
Disease Exacerbation
[description not available]		03.7730
Blood Pressure, Low
[description not available]		02.2510
Hypotension
Abnormally low BLOOD PRESSURE that can result in inadequate blood flow to the brain and other vital organs. Common symptom is DIZZINESS but greater negative impacts on the body occur when there is prolonged depravation of oxygen and nutrients.		02.2510
Drug Overdose
Accidental or deliberate use of a medication or street drug in excess of normal dosage.		02.2510
Diabetic Angiopathies
VASCULAR DISEASES that are associated with DIABETES MELLITUS.		04.5322
Adverse Drug Event
[description not available]		08.1710
Drug-Related Side Effects and Adverse Reactions
Disorders that result from the intended use of PHARMACEUTICAL PREPARATIONS. Included in this heading are a broad variety of chemically-induced adverse conditions due to toxicity, DRUG INTERACTIONS, and metabolic effects of pharmaceuticals.		03.1710
Fasting Hypoglycemia
HYPOGLYCEMIA expressed in the postabsorptive state, after prolonged FASTING, or an overnight fast.		08.2483
Hypoglycemia
A syndrome of abnormally low BLOOD GLUCOSE level. Clinical hypoglycemia has diverse etiologies. Severe hypoglycemia eventually lead to glucose deprivation of the CENTRAL NERVOUS SYSTEM resulting in HUNGER; SWEATING; PARESTHESIA; impaired mental function; SEIZURES; COMA; and even DEATH.		013.2483
Hyperglycemia, Postprandial
Abnormally high BLOOD GLUCOSE level after a meal.		09.48193
Hyperglycemia
Abnormally high BLOOD GLUCOSE level.		09.48193
Lipodystrophy
A collection of heterogenous conditions resulting from defective LIPID METABOLISM and characterized by ADIPOSE TISSUE atrophy. Often there is redistribution of body fat resulting in peripheral fat wasting and central adiposity. They include generalized, localized, congenital, and acquired lipodystrophy.		02.1510
Blood Pressure, High
[description not available]		02.8630
Hypertension
Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.		02.8630
Glycosuria
The appearance of an abnormally large amount of GLUCOSE in the urine, such as more than 500 mg/day in adults. It can be due to HYPERGLYCEMIA or genetic defects in renal reabsorption (RENAL GLYCOSURIA).		015.26202
Weight Reduction
[description not available]		012.3381
Weight Loss
Decrease in existing BODY WEIGHT.		07.3381
Acetonemia
[description not available]		02.1510
Kidney Diseases
Pathological processes of the KIDNEY or its component tissues.		02.8730
Dermatoses
[description not available]		02.5820
Skin Diseases
Diseases involving the DERMIS or EPIDERMIS.		02.5820
Hyperuricemia
Excessive URIC ACID or urate in blood as defined by its solubility in plasma at 37 degrees C; greater than 0.42mmol per liter (7.0mg/dL) in men or 0.36mmol per liter (6.0mg/dL) in women. This condition is caused by overproduction of uric acid or impaired renal clearance. Hyperuricemia can be acquired, drug-induced or genetically determined (LESCH-NYHAN SYNDROME). It is associated with HYPERTENSION and GOUT.		03.0910
Cardiovascular Diseases
Pathological conditions involving the CARDIOVASCULAR SYSTEM including the HEART; the BLOOD VESSELS; or the PERICARDIUM.		04.8721
Bone Fractures
[description not available]		03.1210
Acute Kidney Failure
[description not available]		03.1210
Acidosis, Diabetic
[description not available]		03.1210
Urinary Tract Infections
Inflammatory responses of the epithelium of the URINARY TRACT to microbial invasions. They are often bacterial infections with associated BACTERIURIA and PYURIA.		04.8721
Diabetic Ketoacidosis
A life-threatening complication of diabetes mellitus, primarily of TYPE 1 DIABETES MELLITUS with severe INSULIN deficiency and extreme HYPERGLYCEMIA. It is characterized by KETOSIS; DEHYDRATION; and depressed consciousness leading to COMA.		03.1210
Fractures, Bone
Breaks in bones.		03.1210
Acute Kidney Injury
Abrupt reduction in kidney function. Acute kidney injury encompasses the entire spectrum of the syndrome including acute kidney failure; ACUTE KIDNEY TUBULAR NECROSIS; and other less severe conditions.		03.1210
Vascular Injuries
[description not available]		02.2110
Pulmonary Arterial Remodeling
[description not available]		02.2110
Cirrhosis
[description not available]		02.2110
Fibrosis
Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury.		02.2110
Injury, Myocardial Reperfusion
[description not available]		02.2110
Hyperlipemia
[description not available]		06.46100
Innate Inflammatory Response
[description not available]		07.55120
Hyperlipidemias
Conditions with excess LIPIDS in the blood.		06.46100
Inflammation
A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.		07.55120
Glycosuria, Renal
An autosomal inherited disorder due to defective reabsorption of GLUCOSE by the PROXIMAL RENAL TUBULES. The urinary loss of glucose can reach beyond 50 g/day. It is attributed to the mutations in the SODIUM-GLUCOSE TRANSPORTER 2 encoded by the SLC5A2 gene.		03.9210
Impaired Glucose Tolerance
[description not available]		02.110
Albuminuria
The presence of albumin in the urine, an indicator of KIDNEY DISEASES.		02.110
Glucose Intolerance
A pathological state in which BLOOD GLUCOSE level is less than approximately 140 mg/100 ml of PLASMA at fasting, and above approximately 200 mg/100 ml plasma at 30-, 60-, or 90-minute during a GLUCOSE TOLERANCE TEST. This condition is seen frequently in DIABETES MELLITUS, but also occurs with other diseases and MALNUTRITION.		02.110
Kidney Failure
A severe irreversible decline in the ability of kidneys to remove wastes, concentrate URINE, and maintain ELECTROLYTE BALANCE; BLOOD PRESSURE; and CALCIUM metabolism.		05.7321
Renal Insufficiency
Conditions in which the KIDNEYS perform below the normal level in the ability to remove wastes, concentrate URINE, and maintain ELECTROLYTE BALANCE; BLOOD PRESSURE; and CALCIUM metabolism. Renal insufficiency can be classified by the degree of kidney damage (as measured by the level of PROTEINURIA) and reduction in GLOMERULAR FILTRATION RATE.		05.7321
Choline Deficiency
A condition produced by a deficiency of CHOLINE in animals. Choline is known as a lipotropic agent because it has been shown to promote the transport of excess fat from the liver under certain conditions in laboratory animals. Combined deficiency of choline (included in the B vitamin complex) and all other methyl group donors causes liver cirrhosis in some animals. Unlike compounds normally considered as vitamins, choline does not serve as a cofactor in enzymatic reactions. (From Saunders Dictionary & Encyclopedia of Laboratory Medicine and Technology, 1984)		02.1110
Asymmetric Diabetic Proximal Motor Neuropathy
[description not available]		02.1310
Diabetic Neuropathies
Peripheral, autonomic, and cranial nerve disorders that are associated with DIABETES MELLITUS. These conditions usually result from diabetic microvascular injury involving small blood vessels that supply nerves (VASA NERVORUM). Relatively common conditions which may be associated with diabetic neuropathy include third nerve palsy (see OCULOMOTOR NERVE DISEASES); MONONEUROPATHY; mononeuropathy multiplex; diabetic amyotrophy; a painful POLYNEUROPATHY; autonomic neuropathy; and thoracoabdominal neuropathy. (From Adams et al., Principles of Neurology, 6th ed, p1325)		02.1310
Diabetic Retinopathy
Disease of the RETINA as a complication of DIABETES MELLITUS. It is characterized by the progressive microvascular complications, such as ANEURYSM, interretinal EDEMA, and intraocular PATHOLOGIC NEOVASCULARIZATION.		02.1310
Hyperphagia
Ingestion of a greater than optimal quantity of food.		02.1310
Cirrhoses, Experimental Liver
[description not available]		02.1310
Cancer of Esophagus
[description not available]		02.1310
Esophageal Neoplasms
Tumors or cancer of the ESOPHAGUS.		02.1310
Dermatitis Medicamentosa
[description not available]		03.0610
Encephalopathy, Traumatic
[description not available]		02.1310
Brain Injuries, Traumatic
A form of acquired brain injury which occurs when a sudden trauma causes damage to the brain.		02.1310
Hyponatremia
Deficiency of sodium in the blood; salt depletion. (Dorland, 27th ed)		02.1310
Genital Tract Infections
[description not available]		03.5111
Arterial Diseases, Carotid
[description not available]		03.5111
Carotid Artery Diseases
Pathological conditions involving the CAROTID ARTERIES, including the common, internal, and external carotid arteries. ATHEROSCLEROSIS and TRAUMA are relatively frequent causes of carotid artery pathology.		03.5111
Atherogenesis
[description not available]		02.1510
Atherosclerosis
A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.		02.1510