molecular formula C21H27N5O4S B1671590 Glipizide CAS No. 29094-61-9

Glipizide

货号: B1671590
CAS 编号: 29094-61-9
分子量: 445.5 g/mol
InChI 键: ZJJXGWJIGJFDTL-UHFFFAOYSA-N
注意: 仅供研究使用。不适用于人类或兽医用途。
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描述

格列吡嗪是一种口服降糖药,属于第二代磺酰脲类药物。它主要用于控制2型糖尿病患者的血糖水平。 格列吡嗪通过刺激胰腺释放胰岛素并增加组织对胰岛素的敏感性来发挥作用 . 它首次于1984年上市,并以各种商品名销售,包括Glucotrol .

准备方法

合成路线和反应条件: 格列吡嗪的合成涉及多个步骤,从4-[2-(5-甲基吡嗪-2-甲酰胺)乙基]苯磺酰胺开始。 关键步骤包括氯化,然后在铁催化剂和一氧化碳存在下与环己胺反应 . 该方法简单实用,为格列吡嗪的合成提供了一条新的工艺路线 .

工业生产方法: 在工业生产中,格列吡嗪通常采用溶剂蒸发法制备,以提高其溶解度。格列吡嗪的固体分散体采用聚合物如聚乙烯吡咯烷酮 (PVP) 和聚乙二醇 (PEG) 制备。 药物与聚合物的比例以及溶剂蒸发的条件经过优化,以达到所需的溶解度和溶解速率 .

科学研究应用

Primary Treatment for Type 2 Diabetes

  • Indication : Glipizide is indicated for adults with type 2 diabetes as an adjunct to diet and exercise. It is often prescribed when glycemic control is inadequate with lifestyle modifications alone .
  • Combination Therapy : It can be used in conjunction with other antidiabetic medications like metformin, especially in cases where monotherapy does not achieve desired HbA1c levels .

Efficacy in Glycemic Control

  • In clinical studies, this compound has shown significant reductions in fasting blood glucose and HbA1c levels when used as part of a comprehensive diabetes management plan. A meta-analysis indicated that this compound effectively reduced HbA1c by approximately 1-2% compared to placebo .

Cardiovascular Outcomes

  • Recent studies have evaluated the cardiovascular safety of this compound, particularly in patients with a high risk of cardiovascular disease. While older sulfonylureas were associated with increased cardiovascular risks, newer studies suggest that this compound may have a neutral effect on cardiovascular outcomes, making it a safer option for patients with comorbid conditions .

Case Study 1: Efficacy in Elderly Patients

A study involving elderly patients with type 2 diabetes demonstrated that this compound effectively lowered blood glucose levels while maintaining a favorable safety profile. The patients showed improved glycemic control without significant adverse effects over a six-month period .

Case Study 2: Combination Therapy

In another case study, a patient initially treated with metformin alone was switched to a combination of metformin and this compound after failing to achieve target HbA1c levels. The addition of this compound led to a significant reduction in HbA1c from 8.5% to 6.9% within three months, highlighting its effectiveness as an adjunct therapy .

Side Effects

While this compound is generally well-tolerated, it can cause several side effects:

  • Hypoglycemia : The most common adverse effect, particularly if meals are skipped or if the patient engages in excessive physical activity without adjusting their medication .
  • Gastrointestinal Issues : Nausea, vomiting, and diarrhea can occur but are usually mild and transient .
  • Weight Gain : Some patients may experience weight gain due to increased insulin secretion and decreased glucose utilization by tissues .

作用机制

格列吡嗪通过使胰岛的胰岛β细胞对胰岛素反应敏感而发挥作用。它部分阻断β细胞中的钾通道,导致细胞去极化并打开电压门控钙通道。 由此产生的钙流入促进β细胞释放胰岛素 . 这种机制通过促进胰岛素分泌和增加组织对胰岛素的敏感性来帮助降低血糖水平 .

相似化合物的比较

类似化合物: 格列吡嗪经常与其他磺酰脲类药物如格列美脲和格列本脲进行比较。 它还与非磺酰脲类药物如二甲双胍和胰高血糖素样肽-1 类似物如司美格鲁肽进行比较 .

独特性: 与其他磺酰脲类药物相比,格列吡嗪的吸收和起效速度更快,半衰期最短,作用持续时间最短。 这降低了长时间低血糖的风险,而长时间低血糖常在其他降血糖药物中观察到 . 此外,格列吡嗪独特的化学结构,包括非极性侧链,增强了其降血糖效力 .

生物活性

Glipizide is an oral hypoglycemic agent belonging to the sulfonylurea class, primarily used in the management of type 2 diabetes mellitus (T2DM). Its biological activity involves several mechanisms that contribute to its efficacy in lowering blood glucose levels. This article explores the pharmacodynamics, pharmacokinetics, clinical efficacy, and potential interactions of this compound, supported by data tables and case studies.

This compound functions as an insulin secretagogue , stimulating insulin release from pancreatic beta cells. The primary mechanism involves:

  • Binding to Sulfonylurea Receptors : this compound binds to the sulfonylurea receptor (SUR1) on the beta-cell membrane, leading to the closure of ATP-sensitive potassium channels. This causes depolarization of the cell membrane and opening of voltage-gated calcium channels, resulting in increased intracellular calcium levels and subsequent insulin secretion .
  • Extrapancreatic Effects : Apart from stimulating insulin release, this compound enhances glucose uptake in peripheral tissues such as skeletal muscle and adipose tissue. It also inhibits hepatic glucose output and lipolysis, thereby contributing to overall glucose homeostasis .

Pharmacokinetics

The pharmacokinetic profile of this compound is characterized by:

  • Absorption : this compound is rapidly absorbed after oral administration, with peak plasma concentrations occurring approximately 1-2 hours post-dose.
  • Metabolism : It undergoes extensive hepatic metabolism primarily via cytochrome P450 enzymes (CYP2C9), producing inactive metabolites that are excreted in urine.
  • Half-Life : The elimination half-life ranges from 2 to 4 hours, necessitating multiple daily doses for sustained effect .

Clinical Efficacy

Numerous clinical studies have assessed the efficacy of this compound in managing T2DM. A notable study involved two multicenter clinical trials assessing an extended-release formulation (GITS) of this compound:

Dosage (mg) Fasting Plasma Glucose Reduction (mg/dl) HbA1c Reduction (%)
5-57-1.50
10-65-1.70
20-74-1.82
PlaceboNo significant changeNo significant change

The results indicated that all doses significantly reduced fasting plasma glucose (FPG) and HbA1c compared to placebo, with maximal efficacy observed at doses of 20 mg for FPG and 5 mg for HbA1c .

Case Studies

A multi-center assessment involving 592 patients demonstrated that this compound effectively controlled blood glucose levels in both treatment-naïve and previously treated patients. The study reported:

  • A rapid decrease in post-prandial blood glucose levels within the first week.
  • A mean increase in body weight of approximately 1 kg over 12 weeks.
  • High patient tolerance with only a small percentage (4.7%) experiencing side effects, primarily mild hypoglycemia .

Pharmacogenomic Considerations

Pharmacogenomic studies have highlighted genetic factors influencing this compound efficacy. For instance, variations in genes related to drug metabolism can affect individual responses to this compound treatment, emphasizing the need for personalized medicine approaches in diabetes management .

Herb-Drug Interactions

Recent research has explored potential interactions between this compound and herbal compounds. For example, Andrographis paniculata (APE) was shown to enhance the pharmacokinetic parameters of this compound in diabetic rats, suggesting a synergistic effect that could improve therapeutic outcomes . Conversely, certain herbs may inhibit its metabolism, leading to altered bioavailability and efficacy.

常见问题

Basic Research Questions

Q. What experimental methodologies are recommended for quantifying glipizide in pharmacokinetic studies?

High-performance liquid chromatography (HPLC) with UV detection is widely used due to its specificity and sensitivity. Key parameters include:

  • Column : C18 reverse-phase (e.g., 250 mm × 4.6 mm, 5 µm particle size).
  • Mobile phase : Acetonitrile-phosphate buffer (pH 3.0) in a 40:60 ratio.
  • Flow rate : 1.0 mL/min.
  • Detection wavelength : 225 nm. Validation should follow ICH guidelines for linearity (1–50 µg/mL), precision (RSD <2%), and recovery (>95%) .

Q. How should preclinical studies be designed to evaluate this compound’s mechanism of action in glucose regulation?

  • In vitro : Use pancreatic β-cell lines (e.g., INS-1) to measure insulin secretion under varying glucose concentrations (5–25 mM) with this compound (1–100 nM).
  • In vivo : Employ streptozotocin-induced diabetic rodent models, administering this compound (2.5–10 mg/kg) and monitoring blood glucose via glucometers at 0, 30, 60, and 120 minutes post-dose. Include control groups (vehicle and healthy animals) and validate results with Western blotting for SUR1 receptor expression .

Q. What statistical approaches are appropriate for analyzing this compound’s efficacy in clinical trials?

Use ANOVA for comparing HbA1c reduction across treatment arms (e.g., this compound vs. placebo), followed by post-hoc Tukey tests. For time-series glucose data, mixed-effects models account for intra-patient variability. Sample size calculations should assume a 0.5% HbA1c difference with 80% power and α=0.05 .

Advanced Research Questions

Q. How can contradictory findings on this compound’s cardiovascular risks be resolved in meta-analyses?

  • Data stratification : Separate studies by patient comorbidities (e.g., CVD history) and this compound dosage (≤10 mg/day vs. >10 mg/day).
  • Sensitivity analysis : Exclude trials with high attrition rates (>20%) or unblinded designs.
  • Meta-regression : Investigate confounding variables like concomitant metformin use. Tools like Cochrane’s ROBINS-I should assess bias .

Q. What in silico strategies are effective for predicting this compound-drug interactions at the CYP2C9 enzyme?

  • Molecular docking : Use AutoDock Vina to simulate this compound binding to CYP2C9 (PDB ID: 1OG5).
  • Pharmacophore modeling : Identify critical interaction sites (e.g., sulfonylurea moiety).
  • Machine learning : Train random forest models on datasets like DrugBank to predict inhibition constants (Ki). Validate with in vitro microsomal assays .

Q. How do genetic polymorphisms (e.g., CYP2C9*3) impact this compound pharmacokinetics across diverse populations?

  • Study design : Recruit cohorts stratified by CYP2C9 genotypes (e.g., *1/*1, *1/*3).
  • PK parameters : Calculate AUC0–∞, Cmax, and t1/2 via non-compartmental analysis (WinNonlin).
  • Statistical modeling : Use NONMEM for population PK analysis, incorporating covariates like BMI and renal function. Ethical considerations: Ensure informed consent addresses genetic data privacy .

Q. Methodological Guidance

Q. What criteria define a robust literature review for identifying gaps in this compound research?

  • Search strategy : Combine terms (e.g., “this compound AND pharmacokinetics NOT metformin”) across PubMed, Scopus, and Web of Science, limited to 2010–2025.
  • Screening : PRISMA flowchart to document inclusion/exclusion.
  • Quality assessment : Apply Newcastle-Ottawa Scale for observational studies. Highlight understudied areas (e.g., long-term neurocognitive effects) .

Q. How can researchers optimize this compound formulation stability in dissolution studies?

  • Accelerated stability testing : Store tablets at 40°C/75% RH for 6 months. Monitor degradation products via LC-MS.
  • Dissolution media : Use pH 1.2 (HCl), 4.5 (acetate), and 6.8 (phosphate) to simulate gastrointestinal conditions.
  • Kinetic modeling : Apply Weibull equations to predict shelf-life .

Q. Data Presentation & Reproducibility

Q. What are the best practices for reporting this compound clinical trial data to ensure reproducibility?

  • Raw data : Deposit in repositories like ClinicalTrials.gov or Dryad.
  • Preprocessing : Document outlier removal criteria (e.g., values beyond ±3 SD).
  • Visualization : Use Forest plots for meta-analyses and heatmaps for gene expression correlations. Follow CONSORT guidelines for flow diagrams and EQUATOR Network standards .

Q. How should conflicting in vitro vs. in vivo this compound efficacy data be reconciled?

  • Dose translation : Apply allometric scaling (e.g., body surface area adjustment) between cell culture (µM) and animal models (mg/kg).
  • Tissue distribution : Measure this compound concentrations in pancreatic tissue via LC-MS/MS.
  • Mechanistic studies : Use knockout mice (e.g., SUR1−/−) to isolate target effects .

属性

IUPAC Name

N-[2-[4-(cyclohexylcarbamoylsulfamoyl)phenyl]ethyl]-5-methylpyrazine-2-carboxamide
Source PubChem
URL https://pubchem.ncbi.nlm.nih.gov
Description Data deposited in or computed by PubChem

InChI

InChI=1S/C21H27N5O4S/c1-15-13-24-19(14-23-15)20(27)22-12-11-16-7-9-18(10-8-16)31(29,30)26-21(28)25-17-5-3-2-4-6-17/h7-10,13-14,17H,2-6,11-12H2,1H3,(H,22,27)(H2,25,26,28)
Source PubChem
URL https://pubchem.ncbi.nlm.nih.gov
Description Data deposited in or computed by PubChem

InChI Key

ZJJXGWJIGJFDTL-UHFFFAOYSA-N
Source PubChem
URL https://pubchem.ncbi.nlm.nih.gov
Description Data deposited in or computed by PubChem

Canonical SMILES

CC1=CN=C(C=N1)C(=O)NCCC2=CC=C(C=C2)S(=O)(=O)NC(=O)NC3CCCCC3
Source PubChem
URL https://pubchem.ncbi.nlm.nih.gov
Description Data deposited in or computed by PubChem

Molecular Formula

C21H27N5O4S
Source PubChem
URL https://pubchem.ncbi.nlm.nih.gov
Description Data deposited in or computed by PubChem

DSSTOX Substance ID

DTXSID0040676
Record name Glipizide
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Molecular Weight

445.5 g/mol
Source PubChem
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Physical Description

Solid
Record name Glipizide
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Solubility

>66.8 [ug/mL] (The mean of the results at pH 7.4), 1.64e-02 g/L
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Mechanism of Action

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder with increasing prevalence worldwide. Characterized by higher-than-normal levels of blood glucose, T2DM is a complex disorder that arises from the interaction between genetic, environmental and behavioral risk factors. Insulin is a peptide hormone that plays a critical role in regulating blood glucose levels. In response to high blood glucose levels, insulin promotes the uptake of glucose into the liver, muscle cells, and fat cells for storage. Although there are multiple events occurring that lead to the pathophysiology of T2DM, the disorder mainly involves insulin insensitivity as a result of insulin resistance, declining insulin production, and eventual failure of beta cells of pancreatic islets that normally produce insulin. Early management with lifestyle intervention, such as controlled diet and exercise, is critical in reducing the risk of long-term secondary complications, such as cardiovascular mortality. Glipizide, like other sulfonylurea drugs, is an insulin secretagogue, which works by stimulating the insulin release from the pancreatic beta cells thereby increasing the plasma concentrations of insulin. Thus, the main therapeutic action of the drug depends on the functional beta cells in the pancreatic islets. Sulfonylureas bind to the sulfonylurea receptor expressed on the pancreatic beta-cell plasma membrane, leading to the closure of the ATP-sensitive potassium channel and reduced potassium conductance. This results in depolarization of the pancreatic beta cell and opening of the voltage-sensitive calcium channels, promoting calcium ion influx. Increased intracellular concentrations of calcium ions in beta cells stimulates the secretion, or exocytosis, of insulin granules from the cells. Apart from this main mechanism of action, the blood-glucose-lowering effect of glipizide involves increased peripheral glucose utilization via stimulating hepatic gluconeogenesis and by increasing the number and sensitivity of insulin receptors.
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CAS No.

29094-61-9
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Melting Point

200-203, 208 - 209 °C
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Retrosynthesis Analysis

AI-Powered Synthesis Planning: Our tool employs the Template_relevance Pistachio, Template_relevance Bkms_metabolic, Template_relevance Pistachio_ringbreaker, Template_relevance Reaxys, Template_relevance Reaxys_biocatalysis model, leveraging a vast database of chemical reactions to predict feasible synthetic routes.

One-Step Synthesis Focus: Specifically designed for one-step synthesis, it provides concise and direct routes for your target compounds, streamlining the synthesis process.

Accurate Predictions: Utilizing the extensive PISTACHIO, BKMS_METABOLIC, PISTACHIO_RINGBREAKER, REAXYS, REAXYS_BIOCATALYSIS database, our tool offers high-accuracy predictions, reflecting the latest in chemical research and data.

Strategy Settings

Precursor scoring Relevance Heuristic
Min. plausibility 0.01
Model Template_relevance
Template Set Pistachio/Bkms_metabolic/Pistachio_ringbreaker/Reaxys/Reaxys_biocatalysis
Top-N result to add to graph 6

Feasible Synthetic Routes

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