Cyproheptadine
(Synonyms: 塞庚啶) 目录号 : GC65565
Cyproheptadine HCl(Periactin) is a hydrochloride salt form of cyproheptadine which is a histamine receptor antagonist.
Cas No.:129-03-3
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Cyproheptadine HCl(Periactin) is a hydrochloride salt form of cyproheptadine which is a histamine receptor antagonist.
| Cas No. | 129-03-3 | SDF | Download SDF |
| 别名 | 塞庚啶 | ||
| 分子式 | C21H21N | 分子量 | 287.4 |
| 溶解度 | 储存条件 | Store at -20°C | |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.4795 mL | 17.3974 mL | 34.7947 mL |
| 5 mM | 0.6959 mL | 3.4795 mL | 6.9589 mL |
| 10 mM | 0.3479 mL | 1.7397 mL | 3.4795 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Cyproheptadine : a psychopharmacological treasure trove?
CNS Spectr 2022 Oct;27(5):533-535.PMID:33632345DOI:10.1017/S1092852921000250.
Cyproheptadine has a unique pharmacologic portfolio that speaks to the idea of a pluripotent molecule beyond an antiallergic agent which can expand its therapeutic potential to address a multitude of psychiatric indications. Here, authors touch on the topic with focused literature review of extant evidence.
Hyperthermia and Serotonin: The Quest for a "Better Cyproheptadine"
Int J Mol Sci 2022 Mar 20;23(6):3365.PMID:35328784DOI:10.3390/ijms23063365.
Fine temperature control is essential in homeothermic animals. Both hyper- and hypothermia can have deleterious effects. Multiple, efficient and partly redundant mechanisms of adjusting the body temperature to the value set by the internal thermostat exist. The neural circuitry of temperature control and the neurotransmitters involved are reviewed. The GABAergic inhibitory output from the brain thermostat in the preoptic area POA to subaltern neural circuitry of temperature control (Nucleus Raphe Dorsalis and Nucleus Raphe Pallidus) is a function of the balance between the (opposite) effects mediated by the transient receptor potential receptor TRPM2 and EP3 prostaglandin receptors. Activation of TRPM2-expressing neurons in POA favors hypothermia, while inhibition has the opposite effect. Conversely, EP3 receptors induce elevation in body temperature. Activation of EP3-expressing neurons in POA results in hyperthermia, while inhibition has the opposite effect. Agonists at TRPM2 and/or antagonists at EP3 could be beneficial in hyperthermia control. Activity of the neural circuitry of temperature control is modulated by a variety of 5-HT receptors. Based on the theoretical model presented the "ideal" antidote against serotonin syndrome hyperthermia appears to be an antagonist at the 5-HT receptor subtypes 2, 4 and 6 and an agonist at the receptor subtypes 1, 3 and 7. Very broadly speaking, such a profile translates in a sympatholytic effect. While a compound with such an ideal profile is presently not available, better matches than the conventional antidote Cyproheptadine (used off-label in severe serotonin syndrome cases) appear to be possible and need to be identified.
Cyproheptadine: A Potentially Effective Treatment for Functional Gastrointestinal Disorders in Children
Pediatr Ann 2017 Mar 1;46(3):e120-e125.PMID:28287686DOI:10.3928/19382359-20170213-01.
Functional gastrointestinal disorders (FGIDs) negatively affect children's quality of life and health care costs. It has been proposed that alteration of gut serotonin leads to gastrointestinal dysmotility, visceral hypersensitivity, altered gastrointestinal secretions, and brain-gut dysfunction. Cyproheptadine, a serotonin antagonist, has been shown to be a potentially effective and safe treatment option in children who meet the clinical criteria for FGIDs. Well-designed multicenter trials with long-term follow-up are needed to further investigate its efficacy. [Pediatr Ann. 2017;46(3):e120-e125.].
Effects of Cyproheptadine on Mitral Valve Remodeling and Regurgitation After Myocardial Infarction
J Am Coll Cardiol 2022 Aug 2;80(5):500-510.PMID:35902173DOI:10.1016/j.jacc.2022.05.025.
Background: Ischemic mitral regurgitation (MR) is primarily caused by left ventricle deformation, but leaflet thickening with fibrotic changes are also observed in the valve. Increased levels of 5-hydroxytryptamine (5-HT; ie, serotonin) are described after myocardial infarction (MI); 5-HT can induce valve fibrosis through the 5-HT type 2B receptor (5-HT2BR). Objectives: This study aims to test the hypothesis that post-MI treatment with Cyproheptadine (5-HT2BR antagonist) can prevent ischemic MR by reducing the effect of serotonin on mitral biology. Methods: Thirty-six sheep were divided into 2 groups: inferior MI and inferior MI treated with Cyproheptadine (0.5 mg/kg/d). Animals were followed for 90 days. Blood 5-HT, infarct size, left ventricular volume and function, MR fraction and mitral leaflet size were assessed. In a complementary in vitro study, valvular interstitial cells were exposed to pre-MI and post-MI serum collected from the experimental animals. Results: Increased 5-HT levels were observed after MI in nontreated animals, but not in the group treated with Cyproheptadine. Infarct size was similar in both groups (11 ± 3 g vs 9 ± 5 g; P = 0.414). At 90 days, MR fraction was 16% ± 7% in the MI group vs 2% ± 6% in the Cyproheptadine group (P = 0.0001). The increase in leaflet size following MI was larger in the Cyproheptadine group (+40% ± 9% vs +22% ± 12%; P = 0.001). Mitral interstitial cells overexpressed extracellular matrix genes when treated with post-MI serum, but not when exposed to post-MI serum collected from treated animals. Conclusions: Cyproheptadine given after inferior MI reduces post-MI 5-HT levels, prevents valvular fibrotic remodeling, is associated with larger increase in mitral valve size and less MR.
A Cyproheptadine fatality
J Anal Toxicol 1998 Jan-Feb;22(1):72-4.PMID:9491973DOI:10.1093/jat/22.1.72.
A 28-year-old man was found dead by his girlfriend. No anatomic cause of death was identified at autopsy. The heart-blood ethanol concentration was 0.09 g/dL. Comprehensive testing for abused and therapeutic drugs in the blood and urine identified Cyproheptadine, a serotonin and histamine antagonist. This was one of the medications prescribed for the girlfriend, who admitted that several tablets were missing from the vial. The heart blood contained 0.46 mg/L of Cyproheptadine. A review of the literature indicated that only trace amounts of parent drug are identified in the blood following therapeutic use of Cyproheptadine. Therefore, the medical examiner concluded that the cause of death in this case was ethanol and Cyproheptadine intoxication.