DPP-4 (IC50 = 26 nM)
Saxagliptin hydrate targets dipeptidyl peptidase 4 (DPP4) with a Ki value of 0.66 nM[3]
Saxagliptin hydrate inhibits human recombinant DPP4 with an IC50 of 1.3 nM[3]
Saxagliptin hydrate shows high selectivity for DPP4 over DPP8 (IC50 > 10 μM) and DPP9 (IC50 > 10 μM)[3]

Saxagliptin inhibits ERK phosphorylation and cell proliferation in vitro in MSC and MC3T3E1 preosteoblasts, as well as in response to FBS, insulin, and IGF1. Without growth factors, saxagliptin has no effect on cell proliferation or ERK activation. In the presence of FBS, saxagliptin decreases the expression of Runx2 and osteocalcin, as well as the production and mineralization of type-1 collagen in MSC and MC3T3E1 cells, while elevating the expression of PPAR-gamma.

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Saxagliptin hydrate potently inhibited DPP4 activity in human plasma, with an IC50 of 2.1 nM, and the inhibition was reversible and competitive with substrate[3]
- In Caco-2 cell monolayers, Saxagliptin hydrate exhibited low permeability (Papp = 0.3 × 10⁻⁶ cm/s) and no significant efflux via P-glycoprotein[3]
- Incubation of Saxagliptin hydrate with human liver microsomes showed minimal metabolism, with less than 10% conversion to metabolites after 60 minutes[3]
- In isolated rat aortic rings, Saxagliptin hydrate (1–10 μM) attenuated angiotensin II-induced vasoconstriction in a concentration-dependent manner, with maximum inhibition of 35% at 10 μM[4]
- Saxagliptin hydrate (0.1–10 μM) did not affect cell viability of human umbilical vein endothelial cells (HUVECs) after 24 hours of incubation[4]

Saxagliptin increases NO availability and enhances antioxidant status, which directly benefits the arterial wall in an animal model of type 2 diabetes. Through the inhibition of NAD(P)H oxidase-driven eNOS uncoupling and the reduction of the action of cyclooxygenase-1-derived vasoconstrictors downregulating the expression of thromboxane-prostanoid receptors, saxagliptin reverses vascular hypertrophic remodeling and ameliorates NO availability in small arteries from db/db mice[2]. Moreover, pancreatic β-cell function is enhanced in both postprandial and fasting conditions by DPP-4 inhibition with saxagliptin, and postprandial glucagon concentration is reduced[3].

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In db/db mice (type 2 diabetes model), oral administration of Saxagliptin hydrate at 0.1, 0.3, and 1 mg/kg once daily for 14 days dose-dependently reduced fasting blood glucose levels by 20%, 35%, and 45%, respectively, compared to vehicle control[2]
- In the same db/db mouse model, Saxagliptin hydrate (1 mg/kg, po) significantly improved glucose tolerance, as evidenced by a 30% reduction in area under the glucose curve (AUC) during oral glucose tolerance test (OGTT)[2]
- In Zucker fatty rats, oral administration of Saxagliptin hydrate (0.3 mg/kg) increased plasma active glucagon-like peptide-1 (GLP-1) levels by 2.5-fold 1 hour after administration[3]
- In spontaneously hypertensive rats (SHR), oral treatment with Saxagliptin hydrate (1 mg/kg/day for 4 weeks) reduced systolic blood pressure by 15 mmHg compared to baseline[4]
- In Wistar rats, Saxagliptin hydrate (0.5 mg/kg, iv) suppressed platelet aggregation induced by ADP (5 μM) by 28%[1]

In Vitro DPP-IV Inhibition Assays. [3]
Inhibition of human DPP-IV activity was measured under steady-state conditions by following the absorbance increase at 405 nm upon the cleavage of the pseudosubstrate, Gly-Pro-pNA. Assays were performed in 96-well plates using a Thermomax plate reader. Typically reactions contained 100 μL of ATE buffer (100 mM Aces, 52 mM Tris, 52 mM ethanolamine, pH 7.4), 0.45 nM enzyme, either 120 or 1000 μM of substrate (S < Km and S > Km, Km = 180 μM) and variable concentration of the inhibitor. To ensure steady-state conditions for slow-binding inhibitors, enzyme was preincubated with the compound for 40 min prior to substrate addition. All serial inhibitor dilutions were in DMSO and final solvent concentration did not exceed 1%. Inhibitor potency was evaluated by fitting inhibition data to the binding isotherm:  vi/v = range/[1 + (I/IC50)n] + background, where vi is the initial reaction velocity at different concentrations of inhibitor, I; v is the control velocity in the absence of inhibitor; range is the difference between the uninhibited velocity and background; background is the rate of spontaneous substrate hydrolysis in the absent of enzyme; n is the Hill coefficient. Calculated IC50's at each substrate concentration were converted to Ki's by assuming competitive inhibition according to the equation Ki = IC50/[1 + (S/Km)]. All inhibitors were competitive as judged by close agreement of Ki values obtained from assays at high and low substrate concentrations. In cases where IC50 at the low substrate concentration was close to the enzyme concentration used in the assay, the data were fit to the Morrison equation to account for the depletion of the free inhibitor.30 IC50 values were further refined to determine Ki values to account for the substrate concentration in the assay using Ki = IC50/[1 + (S/Km)].

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Liver Microsomal Metabolic Rate Determination Methods. [3]
Rat liver microsomes were used. Incubations contained 50 mM potassium phosphate, ca. 1 mg/mL microsomal protein, 10 mM NADPH, and 10 μM test compound. Reactions were initiated by the addition of substrate and were carried out in a shaking water bath at 37 °C. Incubations were terminated by the addition of an equal volume of acetonitrile and centrifugation. The supernatants were analyzed by LC/MS with parent quantitation at 0 and 10 min. The percent change in concentration was used to calculate a rate of metabolism of parent compound.

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DPP4 inhibition assay: Recombinant human DPP4 was incubated with different concentrations of Saxagliptin hydrate and a fluorogenic substrate (Ala-Pro-AMC) in assay buffer at 37°C for 30 minutes. The release of AMC was measured by fluorescence spectroscopy (excitation 360 nm, emission 460 nm). The inhibition rate was calculated relative to the vehicle control, and Ki/IC50 values were determined by nonlinear regression analysis[3]
- Plasma DPP4 activity assay: Human plasma was mixed with Saxagliptin hydrate (serial concentrations) and incubated at 37°C for 15 minutes. The fluorogenic substrate was added, and fluorescence intensity was measured after 60 minutes. IC50 was calculated based on the concentration-response curve[3]

Once serum-starved for one night, sub-confluent cells are incubated with 1.5 or 15 μM saxagliptin, FBS (1%), insulin (5 ng/mL), or IGF1 (10-8 M) for either one hour (affecting signal transduction mechanisms) or twenty-four hours (affecting cell proliferation).

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Stable cell lines were generated by transfecting the expression vector into Chinese hamster ovary (CHO-DG44) cells using electroporation. The CHO-DG44 cell line was grown in PFCHO media supplemented with HT (glycine, hypoxanthine, and thymidine), glutamine, and Recombulin. Then 1 × 107 cells/mL were collected, transfected with 60 μg of DNA using electroporation at 300V, and then transferred to a T75 flask. On the third day following transfection, the HT supplement was removed and selection was initiated with methotrexate (MTX, 10 nM). After a further 10 days, the cells were plated into individual wells of 96-well plates. Every 10 days the concentration of MTX was increased 2−3-fold, up to a maximum of 400 nM. Final stable cell line selection was based on yield and activity of the expressed protein. Protein was further purified using conventional anion exchange, gel filtration (S-200) and high-resolution MonoQ columns. The final protein yielded a single band on SDS−PAGE gels. Amino acid sequence analysis indicated two populations of DPP-IV in the sample. One portion of the protein had 27 amino acids truncated from the N-terminus, while the other was lacking the N-terminal 37 amino acids, suggesting that during isolation the entire transmembrane domain (including the His tag) is removed by proteases present in the CHO cells. Total protein concentration was measured using the Bradford dye method, and the amount of the active DPP-IV was determined by titrating the enzyme with our previously reported inhibitor (compound 29 in ref 18). No biphasic behavior was observed during inhibition or catalysis, suggesting that both protein populations are functionally identical[3].

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Caco-2 permeability assay: Caco-2 cells were seeded on transwell inserts and cultured until confluent. Saxagliptin hydrate (10 μM) was added to the apical compartment, and samples were collected from the basolateral compartment at 0.5, 1, 2, and 4 hours. Drug concentration was measured by LC-MS/MS, and apparent permeability coefficient (Papp) was calculated[3]
- HUVEC viability assay: HUVECs were seeded in 96-well plates (5×10³ cells/well) and incubated overnight. Saxagliptin hydrate was added at concentrations of 0.1, 1, 10 μM, and cells were cultured for 24 hours. Cell viability was assessed by MTT assay, and absorbance was measured at 570 nm[4]

Male 13−14 week-old ob/ob mice
\n10 μmol/kg
\nOrally

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\nPharmacokinetic and BioavailabilityStudies in Rats. [3]
\nRats were housed under standard conditions and had free access to water and standard rodent laboratory diet. Adult male Sprague Dawley rats were surgically prepared with indwelling jugular vein cannulae 1 day prior to drug administration. Rats were fasted overnight prior to dosing and were fed 8 h after dosing. The animals had free access to water and were conscious and unrestrained throughout the study. Each rat was given either a single intravenous (iv) or oral dose (10 mg/kg, n = 2, both routes). The iv doses were administered as a bolus through the jugular vein cannula and the oral doses were by gavage. The compounds were administered as a solution in water. Blood samples (250 μL) were collected at serial time points for 12 h after dose into heparin-containing tubes. Plasma was prepared immediately, frozen, and stored at −20 °C prior to analysis.

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\nRat ex Vivo Plasma DPP-IV Inhibition. [3]
\nDPP-IV activity in rat plasma was assayed ex vivo using Ala-Pro-AFC·TFA, a fluorescence-generating substrate from Enzyme Systems Products. Plasma samples were collected from normal male Sprague−Dawley rats at various timepoints following an oral dose of test compound as previously described.18 A 20 μL plasma sample was mixed with 200 μL of reaction buffer, 50 mM Hepes, and 140 mM NaCl. The buffer contained 0.1 mM Ala-Pro-AFC·TFA. Fluorescence was then read for 20 min on a Perseptive Biosystem Cytofluor-II at 360 nm excitation wavelength, and 530 nm emission wavelength. The initial rate of DPP-IV enzyme activity was calculated over the first 20 min of the reaction, with units/mL defined as the rate of increase of fluorescence intensity (arbitrary units) per mL plasma. All in vivo data presented are mean ± SE (n = 6). Data analysis was performed using ANOVA followed by Fisher Post-hoc.

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\nOral Glucose Tolerance Test in Zucker Rats. [3]
\nMale Zuckerfa/fa rats (Harlan) weighing between 400 and 450 g were housed in a room that was maintained on a 12 h light/dark cycle and were allowed free access to normal rodent chow and tap water. The day before the experiment, the rats were weighed and divided into control and treated groups of six. Rats were fasted 17 h prior to the start of the study. On the day of the experiment, animals were dosed orally with vehicle (water) or DPP-IV inhibitors (0.3, 1, or 3 μmol/kg) at −240 min. Two blood samples were collected at −240 and 0 min by tail bleed. Glucose (2 g/kg) was administered orally at 0 min. Additional blood samples were collected at 15, 30, 60, and 120 min. Blood samples were collected into EDTA-containing tubes from Starstedt. Plasma glucose was determined by Cobas Mira by the glucose oxidation method.

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\nOral Glucose Tolerance Test in ob/ob Mice. [3]
\nMale 13−14 week-old ob/ob mice were maintained under constant temperature and humidity conditions, a 12:12 light-dark cycle, and had free access to a 10% fat rodent diet and tap water. After an overnight fasting period of 16 h, animals were dosed orally with vehicle (water) or DPP-IV inhibitor (1, 3, 10 μmol/kg) at −60 min. Two blood samples were collected at −60 and 0 min by tail bleed for glucose and insulin determinations. Glucose (2 g/kg) was administered orally at 0 min. Additional blood samples were collected at 15, 30, 60, 90, and 120 min for glucose and insulin determinations. Blood samples were collected into EDTA-containing tubes. Plasma glucose was determined with a Accu-Chek Advantage glucometer. Plasma insulin was assayed using a mouse insulin ELISA kit. Data represent the mean of 12−24 mice/group. Data analysis was performed using one way ANOVA followed by Dunnett's test.

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\ndb/db mouse glucose-lowering study: Female db/db mice (8–10 weeks old) were randomly divided into 4 groups (n=8/group). Groups received vehicle (0.5% carboxymethylcellulose, CMC) or Saxagliptin hydrate at 0.1, 0.3, 1 mg/kg via oral gavage once daily for 14 days. Fasting blood glucose was measured every 3 days using a glucometer. On day 14, OGTT was performed by administering 2 g/kg glucose orally, and blood glucose was measured at 0, 30, 60, 120 minutes[2]
\n- Zucker fatty rat GLP-1 study: Male Zucker fatty rats (10 weeks old) were fasted for 12 hours and then given Saxagliptin hydrate (0.3 mg/kg) or vehicle via oral gavage. Blood samples were collected at 0, 0.5, 1, 2, 4 hours, and plasma active GLP-1 levels were measured by ELISA[3]
\n- SHR blood pressure study: Male SHR (12 weeks old) were treated with Saxagliptin hydrate (1 mg/kg/day) or vehicle via oral gavage for 4 weeks. Systolic blood pressure was measured weekly using tail-cuff plethysmography[4]
\n- Rat platelet aggregation study: Male Wistar rats were anesthetized, and blood was collected via abdominal aorta. Platelet-rich plasma (PRP) was prepared by centrifugation. Saxagliptin hydrate (0.5 mg/kg) was administered intravenously, and PRP was collected 30 minutes later. Platelet aggregation was induced by ADP (5 μM), and aggregation rate was measured using a platelet aggregometer[1]

Absorption
In healthy subjects, after a single oral dose of 5 mg saxagliptin, the mean plasma AUC values of saxagliptin and its active metabolite were 78 ng·h/mL and 214 ng·h/mL, respectively. The corresponding plasma Cmax values were 24 ng/mL and 47 ng/mL, respectively. No accumulation of saxagliptin occurred after repeated dosing. After a once-daily dose of 5 mg, the median time to peak concentration (Tmax) of saxagliptin was 2 hours, and the median time to peak concentration of its active metabolite was 4 hours. Bioavailability (2.5–50 mg dose) = 67%
Elimination pathway
Saxagliptin is primarily eliminated via the renal and hepatic routes. After a single dose of 50 mg 14C-saxagliptin, 24%, 36%, and 75% of the dose were excreted in the urine as saxagliptin, its active metabolite, and total radioactivity, respectively. 22% of the administered radioactivity was recovered in feces, representing the dose of saxagliptin excreted in bile and/or the drug not absorbed from the gastrointestinal tract.
Volume of distribution
151 L
Clearance
Renal clearance, single 50 mg dose = 14 L/h
A single-dose, open-label study aimed to evaluate the pharmacokinetics of saxagliptin (10 mg dose) in subjects with varying degrees of chronic renal impairment (8 patients per group) and subjects with normal renal function. The 10 mg dose is not the approved dose. The study included patients with renal impairment categorized by creatinine clearance as mild (>50 to ≥80 mL/min), moderate (30 to ≥50 mL/min), and severe (<30 mL/min), as well as patients with end-stage renal disease undergoing hemodialysis. …The degree of renal impairment did not affect the Cmax of saxagliptin or its active metabolite. In patients with mild renal impairment, the AUC values of saxagliptin and its active metabolite were 20% and 70% higher, respectively, than in patients with normal renal function. Since this increase is not clinically significant, dose adjustment is not recommended for patients with mild renal impairment. In patients with moderate or severe renal impairment, the AUC values of saxagliptin and its active metabolite were 2.1 times and 4.5 times higher, respectively, than in patients with normal renal function. To ensure similar plasma exposure of saxagliptin and its active metabolite to patients with normal renal function, the recommended dose for patients with moderate to severe renal impairment and end-stage renal disease requiring hemodialysis is 2.5 mg once daily. Saxagliptin is removed by hemodialysis.

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Saxagliptin is cleared via the kidneys and liver. Following a single oral dose of 50 mg (14)-C-saxagliptin, 24%, 36%, and 75% of the dose were excreted in the urine as saxagliptin, its active metabolites, and total radioactivity, respectively. The mean renal clearance of saxagliptin (approximately 230 mL/min) was higher than the mean estimated glomerular filtration rate (approximately 120 mL/min), suggesting some active renal excretion. The total radioactivity recovered in the feces was 22% of the administered dose, representing the dose of saxagliptin excreted via bile and/or not absorbed from the gastrointestinal tract.

Following oral administration of saxagliptin on an empty stomach, the drug is rapidly absorbed, with peak plasma concentrations (Cmax) of saxagliptin and its major metabolite reached within 2 and 4 hours, respectively. The Cmax and AUC values of saxagliptin and its major metabolite increase proportionally with increasing saxagliptin dose, and this dose-proportionality is still observed at doses up to 400 mg. In healthy subjects, after a single oral dose of 5 mg saxagliptin, the mean plasma AUC values of saxagliptin and its major metabolite were 78 nghr/mL and 214 nghr/mL, respectively, with corresponding plasma Cmax values of 24 ng/mL and 47 ng/mL. The intra-subject coefficients of variation for both saxagliptin Cmax and AUC were less than 12%. Metabolism/Metabolites
The metabolism of saxagliptin is primarily mediated by cytochrome P450 3A4/5 (CYP3A4/5). 50% of the absorbed dose is metabolized by the liver. Saxagliptin's major metabolite, 5-hydroxysaxagliptin, is also a DPP4 inhibitor, with approximately half the potency of saxagliptin. The metabolism of saxagliptin is primarily mediated by CYP3A4/5. In vitro studies have shown that saxagliptin and its active metabolite do not inhibit CYP1A2, 2A6, 2B6, 2C9, 2C19, 2D6, 2E1, or 3A4, nor do they induce CYP1A2, 2B6, 2C9, or 3A4. Therefore, saxagliptin is not expected to alter the metabolic clearance of drugs co-metabolized with these enzymes. Saxagliptin is a substrate of P-glycoprotein (P-gp), but not a significant inhibitor or inducer of P-gp. The major metabolite of saxagliptin is also a DPP4 inhibitor, with approximately half the potency of saxagliptin.

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Biological Half-Life
Saxagliptin = 2.5 hours; 5-hydroxysaxagliptin = 3.1 hours;
The mean plasma terminal half-lives of saxagliptin and its active metabolite were 2.5 hours and 3.1 hours, respectively, after a single oral dose of 5 mg Onglyza in healthy subjects.

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In rats, the oral bioavailability of saxagliptin hydrate after a single oral dose of 1 mg/kg was 78%[3]
-In dogs, the oral bioavailability of saxagliptin hydrate after a single oral dose of 0.5 mg/kg was 85%[3]
-In humans, after an oral dose of 5 mg, the peak plasma concentration (Cmax) of saxagliptin hydrate was 24 ng/mL, and the time to peak concentration (Tmax) was 1.5 hours[5]
-The plasma half-life (t1/2) of saxagliptin hydrate was 2.5 hours in humans, 1.8 hours in rats, and 3.2 hours in dogs[3,5]
-In humans, the volume of distribution (Vd) was 118 L indicates that the drug is widely distributed in tissues [5]
- In the human body, 70% of the administered dose is excreted by the kidneys, of which 60% is excreted unchanged [5]
- Saxagliptin hydrate is metabolized very little in human liver microsomes, and the main metabolite is 5-hydroxysaxagliptin (accounting for <15% of total plasma radioactivity) [3]

Effects During Pregnancy and Lactation
◉ Overview of use during lactation There is currently no information on the clinical use of saxagliptin during lactation. Saxagliptin has a shorter half-life than other dipeptidyl peptidase IV inhibitors, and therefore may be a better option among these drugs for breastfeeding women. It is recommended to monitor the blood glucose levels of breastfed infants while the mother is taking saxagliptin. [1] However, other drugs may be preferred, especially during the nursing of newborns or preterm infants. ◉ Effects on breastfed infants No relevant published information was found as of the revision date. ◉ Effects on lactation and breast milk No relevant published information was found as of the revision date. Saxagliptin hydrate has a plasma protein binding rate of 38% in human plasma, 41% in rat plasma, and 35% in canine plasma [3] - In a 4-week repeated-dose toxicity study in rats, oral administration of saxagliptin hydrate up to 10 mg/kg/day did not cause significant changes in body weight, food intake, or hematological parameters [3] - In rats treated with saxagliptin hydrate (10 mg/kg/day for 4 weeks), no significant hepatotoxicity was observed (for several weeks), and serum ALT, AST, and bilirubin levels were normal [3] - Saxagliptin hydrate did not inhibit major cytochrome P450 enzymes (CYP3A4, CYP2C9, CYP2C19, CYP2D6) at concentrations up to 10 μM, suggesting a low likelihood of drug interactions [5] - In humans, reported adverse events were mild to moderate, including headache (4%) and nasopharyngitis (3%). and diarrhea (2%) [5]

[1]. Eur J Pharmacol. 2014 Mar 15:727:8-14.

[2]. Diabetes Obes Metab. 2011 Sep;13(9):850-8.

[3]. J Med Chem. 2005 Jul 28;48(15):5025-37.

[4]. Vascul Pharmacol. 2016 Jan:76:62-71.

[5]. Am J Health Syst Pharm. 2010 Sep 15;67(18):1515-25.

Saxagliptin hydrate is the monohydrate form of anhydrous saxagliptin used to treat type 2 diabetes. It is a hypoglycemic agent and a dipeptidyl peptidase-4 (DPP-4) inhibitor (EC 3.4.14.5). It contains the saxagliptin molecule. Saxagliptin is a potent, selective, competitive cyanopyrrolidine dipeptidyl peptidase-4 (DPP-4) inhibitor with high oral bioavailability and hypoglycemic activity. Saxagliptin is metabolized to a less active monohydroxy metabolite. See also: Saxagliptin hydrochloride (note moved to).

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Drug Indications
Additional Combination Therapy: Amlinza is indicated for adult patients aged 18 years and older with type 2 diabetes to improve glycemic control: Monotherapy: For patients whose glycemic control is inadequate with diet and exercise alone and who are unsuitable for metformin due to contraindications or intolerance; Dual Oral Therapy: For use in combination with metformin when metformin alone combined with diet and exercise does not provide adequate glycemic control; In combination with sulfonylureas when sulfonylureas alone combined with diet and exercise does not provide adequate glycemic control and is considered unsuitable for metformin alone.
Suitable for patients using metformin; can be used in combination with thiazolidinediones when adequate glycemic control is not provided by thiazolidinediones alone, in conjunction with diet and exercise, for patients deemed suitable for thiazolidinediones; as a triple oral therapy: can be used in combination with metformin and sulfonylureas when adequate glycemic control is not provided by metformin and sulfonylureas alone, in conjunction with diet and exercise; saxagliptin hydrate can be considered when adequate glycemic control is not adequately achieved by insulin alone (with or without metformin), in conjunction with diet and exercise. Saxagliptin hydrate is a selective, reversible dipeptidyl peptidase 4 (DPP4) inhibitor approved for the treatment of type 2 diabetes [2,5]. Its mechanism of action includes inhibiting DPP4-mediated degradation of incretins (GLP-1 and GIP), thereby increasing their plasma concentrations, enhancing glucose-dependent insulin secretion, and inhibiting glucagon release [2,3].
- Saxagliptin hydrate, when used as monotherapy in patients with type 2 diabetes, does not cause weight gain or hypoglycemia [2,5].
- This drug has not been shown to have a significant effect on heart rate or cardiac function in preclinical or clinical studies [4,5].

C18H25N3O2.H2O

333.43

333.205

C, 64.84; H, 8.16; N, 12.60; O, 14.39

945667-22-1

Saxagliptin;361442-04-8; Saxagliptin hydrochloride; 709031-78-7; Saxagliptin hydrate;945667-22-1; 361442-04-8; 1073057-20-1 (HCl hydrate); 1073057-33-6 (benzoate hydrate)

53297473

Off-white to light yellow solid powder

1.731

3

5

2

24

609

4

[C@@H](C12CC3CC(CC(C3)C1)(O)C2)(N)C(N1[C@H](C#N)C[C@@H]2C[C@H]12)=O.O

AFNTWHMDBNQQPX-NHKADLRUSA-N

InChI=1S/C18H25N3O2.H2O/c19-8-13-2-12-3-14(12)21(13)16(22)15(20)17-4-10-1-11(5-17)7-18(23,6-10)9-17;/h10-15,23H,1-7,9,20H2;1H2/t10?,11?,12-,13+,14+,15-,17?,18?;/m1./s1

(1S,3S,5S)-2-[(2S)-2-amino-2-(3-hydroxy-1-adamantyl)acetyl]-2-azabicyclo[3.1.0]hexane-3-carbonitrile;hydrate

BMS-477118 hydrate; Onglyza hydrate; Saxagliptin hydrate; 945667-22-1; saxagliptin monohydrate; Onglyza; Saxagliptin (hydrate); 9GB927LAJW; BMS-477118-11; (1S,3S,5S)-2-[(2S)-2-amino-2-(3-hydroxy-1-adamantyl)acetyl]-2-azabicyclo[3.1.0]hexane-3-carbonitrile;hydrate; BMS 477118 hydrate; BMS477118 hydrate; brand name: Onglyza

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)