Captopril
Vue d'ensemble
Description
Captopril is a potent, competitive inhibitor of angiotensin-converting enzyme (ACE), which is responsible for the conversion of angiotensin I to angiotensin II. Angiotensin II is a key regulator of blood pressure and a critical component of the renin-angiotensin-aldosterone system (RAAS). This compound is primarily used for the management of essential or renovascular hypertension, congestive heart failure, left ventricular dysfunction following myocardial infarction, and nephropathy .
Mécanisme D'action
Biochemical Pathways
The primary biochemical pathway affected by captopril is the renin-angiotensin-aldosterone system (RAAS) . By inhibiting ACE, this compound prevents the formation of angiotensin II, a potent vasoconstrictor. This leads to vasodilation, a decrease in total peripheral resistance, and ultimately, a reduction in blood pressure . Additionally, by reducing angiotensin II levels, this compound decreases aldosterone secretion, which reduces sodium and water reabsorption, further contributing to the antihypertensive effect .
Pharmacokinetics
This compound exhibits favorable pharmacokinetic properties. It has a bioavailability of approximately 70-75% , and peak blood concentrations are reached about 45 to 60 minutes after oral administration . The elimination half-life of unchanged this compound is approximately 1.9 hours , and the primary route of elimination is the kidney . The renal clearance of unchanged this compound exceeds the glomerular filtration rate, due to active tubular secretion of the drug .
Action Environment
The efficacy and stability of this compound can be influenced by various environmental factors. For instance, the co-administration of food or antacids with this compound has been shown to diminish the bioavailability of the latter . Furthermore, this compound’s action can be affected by the patient’s renal function, with patients with chronic renal failure demonstrating longer half-lives compared to normal subjects .
Applications De Recherche Scientifique
Captopril has a wide range of scientific research applications. In chemistry, it is used as a model compound for studying enzyme inhibition and reaction mechanisms. In biology, this compound is used to investigate the role of the renin-angiotensin-aldosterone system in various physiological processes. In medicine, this compound is extensively studied for its therapeutic effects in treating hypertension, heart failure, and diabetic nephropathy .
Analyse Biochimique
Biochemical Properties
Captopril plays a crucial role in biochemical reactions by inhibiting the angiotensin-converting enzyme (ACE). This enzyme is responsible for converting angiotensin I to angiotensin II, a potent vasoconstrictor. By inhibiting ACE, this compound reduces the levels of angiotensin II, leading to vasodilation and decreased blood pressure . This compound interacts with several biomolecules, including ACE, bradykinin, and prostaglandins. The interaction with ACE involves the binding of this compound’s thiol group to the zinc ion at the active site of the enzyme, thereby inhibiting its activity .
Cellular Effects
This compound has significant effects on various cell types and cellular processes. It influences cell function by modulating cell signaling pathways, gene expression, and cellular metabolism. For instance, this compound has been shown to increase cell viability and reduce oxidative stress in C6 cells by decreasing levels of inflammatory markers such as NF-kB, IL-1β, COX-1, and COX-2 . Additionally, this compound can affect the renin-angiotensin-aldosterone system (RAAS), leading to changes in gene expression related to blood pressure regulation and fluid balance .
Molecular Mechanism
The molecular mechanism of this compound involves its competitive inhibition of the angiotensin-converting enzyme (ACE). This compound binds to the active site of ACE, preventing the conversion of angiotensin I to angiotensin II . This inhibition results in decreased vasoconstriction and reduced aldosterone secretion, leading to lower blood pressure. Furthermore, this compound prevents the degradation of vasodilatory prostaglandins, promoting systemic vasodilation .
Temporal Effects in Laboratory Settings
In laboratory settings, the effects of this compound can change over time. This compound is known to have a relatively short half-life of approximately 2 hours . Its stability and degradation can influence its long-term effects on cellular function. Studies have shown that this compound can reduce inflammation and oxidative stress over extended periods, contributing to its protective effects in conditions such as radiation-induced lung injury .
Dosage Effects in Animal Models
The effects of this compound vary with different dosages in animal models. At therapeutic doses, this compound effectively reduces blood pressure and improves cardiac function . At higher doses, this compound can cause adverse effects such as hypotension, renal impairment, and hyperkalemia . In animal models, this compound has been shown to mitigate radiation-induced lung injury and improve survival rates .
Metabolic Pathways
This compound is involved in several metabolic pathways, primarily related to the renin-angiotensin-aldosterone system (RAAS). It inhibits the conversion of angiotensin I to angiotensin II, reducing vasoconstriction and aldosterone secretion . Additionally, this compound can influence the kallikrein-kinin-prostaglandin system, affecting prostaglandin production and renal hemodynamics .
Transport and Distribution
This compound is well-distributed within tissues and is primarily metabolized by the liver . It is excreted unchanged in the urine, with a bioavailability of 70-75% . This compound binds to plasma proteins and can form mixed disulfides with endogenous thiol-containing compounds such as cysteine and glutathione .
Subcellular Localization
This compound’s subcellular localization is influenced by its interactions with specific biomolecules and enzymes. It targets the angiotensin-converting enzyme (ACE) located on the surface of endothelial cells . The thiol group of this compound allows it to bind to the active site of ACE, inhibiting its activity and preventing the conversion of angiotensin I to angiotensin II .
Méthodes De Préparation
Synthetic Routes and Reaction Conditions: Captopril can be synthesized through several methods. One common method involves the reaction of L-proline with 2-methyl-3-mercaptopropionyl chloride in the presence of a base such as triethylamine. The reaction is typically carried out in an organic solvent like dichloromethane at low temperatures to prevent side reactions .
Industrial Production Methods: Industrial production of this compound often involves the use of large-scale reactors where the reaction conditions are carefully controlled to ensure high yield and purity. The process includes steps like recrystallization to purify the final product. The use of advanced techniques such as continuous flow reactors can enhance the efficiency and scalability of the production process .
Analyse Des Réactions Chimiques
Types of Reactions: Captopril undergoes various chemical reactions, including oxidation, reduction, and substitution. For instance, the thiol group in this compound can be oxidized to form disulfides, while the carboxyl group can participate in esterification reactions .
Common Reagents and Conditions: Common reagents used in the reactions involving this compound include oxidizing agents like hydrogen peroxide for oxidation reactions and reducing agents like sodium borohydride for reduction reactions. The reactions are typically carried out under mild conditions to prevent degradation of the compound .
Major Products Formed: The major products formed from these reactions include this compound disulfide from oxidation and various esters from esterification reactions. These derivatives can have different pharmacological properties and are often studied for their potential therapeutic applications .
Comparaison Avec Des Composés Similaires
Captopril is often compared with other ACE inhibitors such as enalapril, lisinopril, and ramipril. While all these compounds inhibit the same enzyme, this compound is unique due to its thiol group, which contributes to its high potency and rapid onset of action. this thiol group can also cause side effects such as skin rashes and taste disturbances, which are less common with other ACE inhibitors .
List of Similar Compounds:- Enalapril
- Lisinopril
- Ramipril
- Benazepril
This compound’s unique structure and rapid action make it a valuable therapeutic agent, despite its potential side effects. Its discovery and development have significantly advanced the treatment of cardiovascular diseases .
Propriétés
IUPAC Name |
(2S)-1-[(2S)-2-methyl-3-sulfanylpropanoyl]pyrrolidine-2-carboxylic acid |
Source
|
|---|---|---|
| Source | PubChem | |
| URL | https://pubchem.ncbi.nlm.nih.gov | |
| Description | Data deposited in or computed by PubChem | |
InChI |
InChI=1S/C9H15NO3S/c1-6(5-14)8(11)10-4-2-3-7(10)9(12)13/h6-7,14H,2-5H2,1H3,(H,12,13)/t6-,7+/m1/s1 |
Source
|
| Source | PubChem | |
| URL | https://pubchem.ncbi.nlm.nih.gov | |
| Description | Data deposited in or computed by PubChem | |
InChI Key |
FAKRSMQSSFJEIM-RQJHMYQMSA-N |
Source
|
| Source | PubChem | |
| URL | https://pubchem.ncbi.nlm.nih.gov | |
| Description | Data deposited in or computed by PubChem | |
Canonical SMILES |
CC(CS)C(=O)N1CCCC1C(=O)O |
Source
|
| Source | PubChem | |
| URL | https://pubchem.ncbi.nlm.nih.gov | |
| Description | Data deposited in or computed by PubChem | |
Isomeric SMILES |
C[C@H](CS)C(=O)N1CCC[C@H]1C(=O)O |
Source
|
| Source | PubChem | |
| URL | https://pubchem.ncbi.nlm.nih.gov | |
| Description | Data deposited in or computed by PubChem | |
Molecular Formula |
C9H15NO3S |
Source
|
| Source | PubChem | |
| URL | https://pubchem.ncbi.nlm.nih.gov | |
| Description | Data deposited in or computed by PubChem | |
Related CAS |
1253948-36-5 |
Source
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| Record name | L-Proline, 1-[(2S)-3-mercapto-2-methyl-1-oxopropyl]-, homopolymer | |
| Source | CAS Common Chemistry | |
| URL | https://commonchemistry.cas.org/detail?cas_rn=1253948-36-5 | |
| Description | CAS Common Chemistry is an open community resource for accessing chemical information. Nearly 500,000 chemical substances from CAS REGISTRY cover areas of community interest, including common and frequently regulated chemicals, and those relevant to high school and undergraduate chemistry classes. This chemical information, curated by our expert scientists, is provided in alignment with our mission as a division of the American Chemical Society. | |
| Explanation | The data from CAS Common Chemistry is provided under a CC-BY-NC 4.0 license, unless otherwise stated. | |
DSSTOX Substance ID |
DTXSID1037197 |
Source
|
| Record name | Captopril | |
| Source | EPA DSSTox | |
| URL | https://comptox.epa.gov/dashboard/DTXSID1037197 | |
| Description | DSSTox provides a high quality public chemistry resource for supporting improved predictive toxicology. | |
Molecular Weight |
217.29 g/mol |
Source
|
| Source | PubChem | |
| URL | https://pubchem.ncbi.nlm.nih.gov | |
| Description | Data deposited in or computed by PubChem | |
Physical Description |
Solid |
Source
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| Record name | Captopril | |
| Source | Human Metabolome Database (HMDB) | |
| URL | http://www.hmdb.ca/metabolites/HMDB0015328 | |
| Description | The Human Metabolome Database (HMDB) is a freely available electronic database containing detailed information about small molecule metabolites found in the human body. | |
| Explanation | HMDB is offered to the public as a freely available resource. Use and re-distribution of the data, in whole or in part, for commercial purposes requires explicit permission of the authors and explicit acknowledgment of the source material (HMDB) and the original publication (see the HMDB citing page). We ask that users who download significant portions of the database cite the HMDB paper in any resulting publications. | |
Solubility |
Freely soluble, Freely soluble in water (approximately 160 mg/mL), Freely soluble in alcohol, chloroform, methylene chloride; sparingly soluble in ethyl acetate, 4.52e+00 g/L |
Source
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| Record name | Captopril | |
| Source | DrugBank | |
| URL | https://www.drugbank.ca/drugs/DB01197 | |
| Description | The DrugBank database is a unique bioinformatics and cheminformatics resource that combines detailed drug (i.e. chemical, pharmacological and pharmaceutical) data with comprehensive drug target (i.e. sequence, structure, and pathway) information. | |
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| Record name | Captopril | |
| Source | Hazardous Substances Data Bank (HSDB) | |
| URL | https://pubchem.ncbi.nlm.nih.gov/source/hsdb/6527 | |
| Description | The Hazardous Substances Data Bank (HSDB) is a toxicology database that focuses on the toxicology of potentially hazardous chemicals. It provides information on human exposure, industrial hygiene, emergency handling procedures, environmental fate, regulatory requirements, nanomaterials, and related areas. The information in HSDB has been assessed by a Scientific Review Panel. | |
| Record name | Captopril | |
| Source | Human Metabolome Database (HMDB) | |
| URL | http://www.hmdb.ca/metabolites/HMDB0015328 | |
| Description | The Human Metabolome Database (HMDB) is a freely available electronic database containing detailed information about small molecule metabolites found in the human body. | |
| Explanation | HMDB is offered to the public as a freely available resource. Use and re-distribution of the data, in whole or in part, for commercial purposes requires explicit permission of the authors and explicit acknowledgment of the source material (HMDB) and the original publication (see the HMDB citing page). We ask that users who download significant portions of the database cite the HMDB paper in any resulting publications. | |
Mechanism of Action |
There are two isoforms of ACE: the somatic isoform, which exists as a glycoprotein comprised of a single polypeptide chain of 1277; and the testicular isoform, which has a lower molecular mass and is thought to play a role in sperm maturation and binding of sperm to the oviduct epithelium. Somatic ACE has two functionally active domains, N and C, which arise from tandem gene duplication. Although the two domains have high sequence similarity, they play distinct physiological roles. The C-domain is predominantly involved in blood pressure regulation while the N-domain plays a role in hematopoietic stem cell differentiation and proliferation. ACE inhibitors bind to and inhibit the activity of both domains, but have much greater affinity for and inhibitory activity against the C-domain. Captopril, one of the few ACE inhibitors that is not a prodrug, competes with ATI for binding to ACE and inhibits and enzymatic proteolysis of ATI to ATII. Decreasing ATII levels in the body decreases blood pressure by inhibiting the pressor effects of ATII as described in the Pharmacology section above. Captopril also causes an increase in plasma renin activity likely due to a loss of feedback inhibition mediated by ATII on the release of renin and/or stimulation of reflex mechanisms via baroreceptors. Captopril’s affinity for ACE is approximately 30,000 times greater than that of ATI., The local role of the renin angiotensin system (RAS) was documented recently beside its conventional systemic functions. Studies showed that the effector angiotensin II (AngII) alters bone health, while inhibition of the angiotensin converting enzyme (ACE-1) preserved these effects. The newly identified Ang1-7 exerts numerous beneficial effects opposing the AngII. Thus, the current study examines the role of Ang1-7 in mediating the osteo-preservative effects of ACEI (captopril) through the G-protein coupled Mas receptor using an ovariectomized (OVX) rat model of osteoporosis. 8 weeks after the surgical procedures, captopril was administered orally (40 mg/kg/day), while the specific Mas receptor blocker (A-779) was delivered at infusion rate of 400 ng/kg/1 min for 6 weeks. Bone metabolic markers were measured in serum and urine. Minerals concentrations were quantified in serum, urine and femoral bones by inductive coupled plasma mass spectroscopy (ICP-MS). Trabecular and cortical morphometry was analyzed in the right distal femurs using micro-CT. Finally, the expressions of RAS peptides, enzymes and receptors along with the receptor activator of NF-kappaB ligand (RANKL) and osteoprotegerin (OPG) were determined femurs heads. OVX animals markedly showed altered bone metabolism and mineralization along with disturbed bone micro-structure. Captopril significantly restored the metabolic bone bio-markers and corrected Ca2+ and P values in urine and bones of estrogen deficient rats. Moreover, the trabecular and cortical morphometric features were repaired by captopril in OVX groups. Captopril also improved the expressions of ACE-2, Ang1-7, Mas and OPG, while abolished OVX-induced up-regulation of ACE-1, AngII, Ang type 1 receptor (AT1R) and RANKL. Inhibition of Ang1-7 cascade by A-779 significantly eradicated captopril protective effects on bone metabolism, mineralization and micro-structure. A-779 also restored OVX effects on RANKL expression and ACE-1/AngII/AT1R cascade and down-regulated OPG expression and ACE-2/Ang1-7/Mas pathway. In line with the clinical observations of the bone-preservative properties following ACE-1 inhibition, local activation of ACE-2/Ang1-7/Mas signaling and suppressed osteoclastogenesis seem responsible for the osteo-preservative effect of captopril, which could offers a potential therapeutic value in treatment of disabling bone and skeletal muscular diseases. |
Source
|
| Record name | Captopril | |
| Source | DrugBank | |
| URL | https://www.drugbank.ca/drugs/DB01197 | |
| Description | The DrugBank database is a unique bioinformatics and cheminformatics resource that combines detailed drug (i.e. chemical, pharmacological and pharmaceutical) data with comprehensive drug target (i.e. sequence, structure, and pathway) information. | |
| Explanation | Creative Common's Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/legalcode) | |
| Record name | Captopril | |
| Source | Hazardous Substances Data Bank (HSDB) | |
| URL | https://pubchem.ncbi.nlm.nih.gov/source/hsdb/6527 | |
| Description | The Hazardous Substances Data Bank (HSDB) is a toxicology database that focuses on the toxicology of potentially hazardous chemicals. It provides information on human exposure, industrial hygiene, emergency handling procedures, environmental fate, regulatory requirements, nanomaterials, and related areas. The information in HSDB has been assessed by a Scientific Review Panel. | |
Color/Form |
White to off-white, crystalline powder, Crystals from ethyl acetate/hexane | |
CAS No. |
62571-86-2 |
Source
|
| Record name | Captopril | |
| Source | CAS Common Chemistry | |
| URL | https://commonchemistry.cas.org/detail?cas_rn=62571-86-2 | |
| Description | CAS Common Chemistry is an open community resource for accessing chemical information. Nearly 500,000 chemical substances from CAS REGISTRY cover areas of community interest, including common and frequently regulated chemicals, and those relevant to high school and undergraduate chemistry classes. This chemical information, curated by our expert scientists, is provided in alignment with our mission as a division of the American Chemical Society. | |
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| Record name | Captopril [USAN:USP:INN:BAN:JAN] | |
| Source | ChemIDplus | |
| URL | https://pubchem.ncbi.nlm.nih.gov/substance/?source=chemidplus&sourceid=0062571862 | |
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| Record name | Captopril | |
| Source | DrugBank | |
| URL | https://www.drugbank.ca/drugs/DB01197 | |
| Description | The DrugBank database is a unique bioinformatics and cheminformatics resource that combines detailed drug (i.e. chemical, pharmacological and pharmaceutical) data with comprehensive drug target (i.e. sequence, structure, and pathway) information. | |
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| Record name | captopril | |
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| Record name | Captopril | |
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| Record name | Captopril | |
| Source | European Chemicals Agency (ECHA) | |
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| Record name | CAPTOPRIL | |
| Source | FDA Global Substance Registration System (GSRS) | |
| URL | https://gsrs.ncats.nih.gov/ginas/app/beta/substances/9G64RSX1XD | |
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| Record name | Captopril | |
| Source | Hazardous Substances Data Bank (HSDB) | |
| URL | https://pubchem.ncbi.nlm.nih.gov/source/hsdb/6527 | |
| Description | The Hazardous Substances Data Bank (HSDB) is a toxicology database that focuses on the toxicology of potentially hazardous chemicals. It provides information on human exposure, industrial hygiene, emergency handling procedures, environmental fate, regulatory requirements, nanomaterials, and related areas. The information in HSDB has been assessed by a Scientific Review Panel. | |
| Record name | Captopril | |
| Source | Human Metabolome Database (HMDB) | |
| URL | http://www.hmdb.ca/metabolites/HMDB0015328 | |
| Description | The Human Metabolome Database (HMDB) is a freely available electronic database containing detailed information about small molecule metabolites found in the human body. | |
| Explanation | HMDB is offered to the public as a freely available resource. Use and re-distribution of the data, in whole or in part, for commercial purposes requires explicit permission of the authors and explicit acknowledgment of the source material (HMDB) and the original publication (see the HMDB citing page). We ask that users who download significant portions of the database cite the HMDB paper in any resulting publications. | |
Melting Point |
103-104, 103-104 °C, 106 °C |
Source
|
| Record name | Captopril | |
| Source | DrugBank | |
| URL | https://www.drugbank.ca/drugs/DB01197 | |
| Description | The DrugBank database is a unique bioinformatics and cheminformatics resource that combines detailed drug (i.e. chemical, pharmacological and pharmaceutical) data with comprehensive drug target (i.e. sequence, structure, and pathway) information. | |
| Explanation | Creative Common's Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/legalcode) | |
| Record name | Captopril | |
| Source | Hazardous Substances Data Bank (HSDB) | |
| URL | https://pubchem.ncbi.nlm.nih.gov/source/hsdb/6527 | |
| Description | The Hazardous Substances Data Bank (HSDB) is a toxicology database that focuses on the toxicology of potentially hazardous chemicals. It provides information on human exposure, industrial hygiene, emergency handling procedures, environmental fate, regulatory requirements, nanomaterials, and related areas. The information in HSDB has been assessed by a Scientific Review Panel. | |
| Record name | Captopril | |
| Source | Human Metabolome Database (HMDB) | |
| URL | http://www.hmdb.ca/metabolites/HMDB0015328 | |
| Description | The Human Metabolome Database (HMDB) is a freely available electronic database containing detailed information about small molecule metabolites found in the human body. | |
| Explanation | HMDB is offered to the public as a freely available resource. Use and re-distribution of the data, in whole or in part, for commercial purposes requires explicit permission of the authors and explicit acknowledgment of the source material (HMDB) and the original publication (see the HMDB citing page). We ask that users who download significant portions of the database cite the HMDB paper in any resulting publications. | |
Synthesis routes and methods
Procedure details
Retrosynthesis Analysis
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Strategy Settings
| Precursor scoring | Relevance Heuristic |
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| 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
Q1: What is the primary mechanism of action of Captopril?
A1: this compound exerts its primary antihypertensive effect by inhibiting the angiotensin-converting enzyme (ACE). [, , , , , , , ] This enzyme catalyzes the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. By blocking this conversion, this compound reduces vasoconstriction, leading to a decrease in blood pressure. [, , , , , ]
Q2: Does this compound impact the renin-angiotensin system (RAS) beyond ACE inhibition?
A2: Yes, research suggests that this compound can influence the RAS in various ways. For instance, it has been shown to increase plasma renin activity (PRA), likely as a compensatory response to reduced angiotensin II levels. [, , , , ] Additionally, chronic this compound treatment can lead to changes in the expression of components of the tissue RAS, such as angiotensinogen in the kidneys. []
Q3: How does this compound impact the nervous system in the context of hypertension?
A4: Studies in spontaneously hypertensive rats (SHR) have shown that chronic this compound treatment can alter the properties of cardiovascular neurons in the rostral ventrolateral medulla (RVL), a brainstem region involved in blood pressure regulation. [] These changes appear to contribute to the long-term blood pressure-lowering effects of this compound. []
Q4: Can this compound cross the blood-brain barrier and directly affect the central nervous system?
A5: While this compound's ability to cross the blood-brain barrier is limited, research in pregnant sheep suggests that it might cross the placenta and directly influence the fetal renin-angiotensin system. [] This finding highlights the complex interplay between this compound and the RAS in different physiological contexts.
Q5: What is the molecular formula and weight of this compound?
A5: this compound has the molecular formula C9H15NO3S and a molecular weight of 217.29 g/mol.
Q6: Is there information available regarding the spectroscopic data or material compatibility of this compound within the provided research?
A6: The provided research focuses primarily on the pharmacological and physiological effects of this compound. It does not delve into detailed spectroscopic data or material compatibility assessments.
Q7: How is this compound absorbed and metabolized in the body?
A8: this compound is rapidly absorbed after oral administration, reaching peak plasma concentrations within approximately 1 hour. [, ] It is primarily metabolized in the liver, forming several metabolites, including this compound-cysteine disulfide. []
Q8: What is the elimination half-life of this compound?
A9: The elimination half-life of this compound is relatively short, ranging from approximately 0.7 to 2 hours. [, ] This short half-life necessitates multiple daily doses to maintain therapeutic effects in most patients. [, ]
Q9: How is this compound's efficacy assessed in preclinical and clinical settings?
A11: Preclinical studies often utilize animal models, such as spontaneously hypertensive rats (SHR), to investigate this compound's effects on blood pressure, organ damage, and other physiological parameters. [, , , , ] Clinical trials typically assess this compound's efficacy in humans with hypertension by monitoring blood pressure changes, 24-hour ambulatory blood pressure monitoring, and evaluating its impact on cardiovascular outcomes. [, , , , , ]
Q10: Does this compound exhibit any direct effects on blood vessels?
A12: Research suggests that this compound might exert direct effects on blood vessels. For instance, studies in atherosclerotic rabbits demonstrated that this compound, as well as the angiotensin II type 1 receptor blocker Valsartan, could inhibit the thickening of the abdominal aorta. []
Q11: Does this compound influence cell proliferation or apoptosis?
A13: Some evidence points to a potential role of this compound in modulating cell proliferation and apoptosis. A study in spontaneously hypertensive rats found that this compound treatment could reverse the increased expression of the pro-apoptotic protein Bax and the decreased expression of the anti-apoptotic protein Bcl-2 in capillary endothelial cells of the heart and brain. [] These findings suggest that this compound may exert protective effects on the vasculature, potentially influencing cell survival pathways.
Q12: Can this compound impact other organ systems beyond the cardiovascular system?
A14: Yes, research indicates that this compound might have effects beyond blood pressure regulation. For example, it has been explored for its potential to improve wound healing in diabetic rats, possibly by increasing nitric oxide and vascular endothelial growth factor (VEGF) levels in wound fluid. []
Q13: What are the common side effects associated with this compound?
A13: While this document focuses on the scientific aspects of this compound, it is essential to acknowledge that side effects can occur with its use. Please consult relevant clinical resources for comprehensive information on this aspect.
Q14: Are there any specific drug delivery systems or targeting strategies being investigated for this compound?
A14: The provided research primarily focuses on traditional oral administration of this compound. While targeted drug delivery holds potential for enhancing efficacy and minimizing off-target effects, the provided literature does not delve into specific strategies for this compound.
Q15: What analytical methods are commonly used to measure this compound levels?
A18: Various analytical techniques can be employed to quantify this compound levels in biological samples. The provided research mentions high-pressure liquid chromatography coupled with mass spectrometry (LC-MS/MS) as a sensitive and specific method for measuring this compound concentrations in plasma. []
Q16: What were some of the key milestones in the development and use of this compound?
A20: this compound was the first clinically approved ACE inhibitor, representing a significant advancement in the treatment of hypertension. [] Its development stemmed from research on peptides isolated from the venom of the Brazilian pit viper Bothrops jararaca, which were found to inhibit ACE. This discovery paved the way for the development of a new class of antihypertensive drugs that revolutionized cardiovascular medicine.
Q17: Does this compound find applications beyond its primary use in hypertension?
A17: Yes, in addition to its well-established role in hypertension management, this compound has been investigated for its potential in other areas, including:
- Heart Failure: this compound has been shown to improve symptoms, reduce hospitalization rates, and enhance survival in patients with heart failure. [, , ]
- Diabetic Nephropathy: Studies suggest that this compound can slow the progression of kidney disease in individuals with diabetes. []
- Myocardial Infarction: Research indicates that early administration of this compound after a heart attack can improve long-term survival and reduce the risk of heart failure. [, ]
- Pulmonary Hypertension: Although less commonly used, this compound has been explored as a treatment option for certain types of pulmonary hypertension. []
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Veuillez noter que tous les articles et informations sur les produits présentés sur BenchChem sont destinés uniquement à des fins informatives. Les produits disponibles à l'achat sur BenchChem sont spécifiquement conçus pour des études in vitro, qui sont réalisées en dehors des organismes vivants. Les études in vitro, dérivées du terme latin "in verre", impliquent des expériences réalisées dans des environnements de laboratoire contrôlés à l'aide de cellules ou de tissus. Il est important de noter que ces produits ne sont pas classés comme médicaments et n'ont pas reçu l'approbation de la FDA pour la prévention, le traitement ou la guérison de toute condition médicale, affection ou maladie. Nous devons souligner que toute forme d'introduction corporelle de ces produits chez les humains ou les animaux est strictement interdite par la loi. Il est essentiel de respecter ces directives pour assurer la conformité aux normes légales et éthiques en matière de recherche et d'expérimentation.
![S-[(2R,3S,4S,6S)-6-[[(2R,3S,4S,5R,6R)-5-[(2S,4S,5S)-5-(ethylamino)-4-methoxyoxan-2-yl]oxy-4-hydroxy-6-[[(2S,5Z,9R,13Z)-9-hydroxy-12-(methoxycarbonylamino)-13-[2-(methyltrisulfanyl)ethylidene]-11-oxo-2-bicyclo[7.3.1]trideca-1(12),5-dien-3,7-diynyl]oxy]-2-methyloxan-3-yl]amino]oxy-4-hydroxy-2-methyloxan-3-yl] 4-[(2S,3R,4R,5S,6S)-3,5-dihydroxy-4-methoxy-6-methyloxan-2-yl]oxy-5-iodo-2,3-dimethoxy-6-methylbenzenecarbothioate](/img/structure/B1668231.png)
