Budesonide

别名:
目录号: V1704 纯度: ≥98%
布地奈德(Rhinocort;Budicort;Entocort;Rhinosol;Pulmicort;Symbicort;Noex Entocort EC)是一种合成糖皮质激素类固醇,被批准用于治疗炎症性疾病,如哮喘、非感染性鼻炎和鼻息肉病。
Budesonide CAS号: 51333-22-3
产品类别: Calcium Channel
产品仅用于科学研究,不针对患者销售
规格 价格 库存 数量
50mg
100mg
250mg
500mg
1g
2g
Other Sizes

Other Forms of Budesonide:

  • [ 2H8 ]-布地奈德
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InvivoChem产品被CNS等顶刊论文引用
纯度/质量控制文件

纯度: ≥98%

产品描述
布地奈德(Rhinocort;Budicort;Entocort;Rhinosol;Pulmicort;Symbicort;Noex Entocort EC)是一种合成糖皮质激素类固醇,被批准用于治疗炎症性疾病,如哮喘、非感染性鼻炎和鼻息肉病。此外,它还用于治疗克罗恩病(炎症性肠病)。
生物活性&实验参考方法
体外研究 (In Vitro)
在 CV-1 细胞中,布地奈德优先结合人糖皮质激素受体(hGR;EC50=45.7 pM),而不是盐皮质激素受体(EC50=7,620 pM)。在巨噬细胞(RAW 264.7 细胞)中,布地奈德(LPS 前 30 分钟)可抑制 LPS (100 ng/mL) + ATP (5 mM) 激活 NLRP3 炎症小体[2]。
体内研究 (In Vivo)
布地奈德(2.0 mg/kg;通过饮食口服;处死前 2、7 和 21 天)可减小肺肿瘤大小[3]。布地奈德预处理(0.5 mg/kg;LPS 注射 (5 mg/kg) 前 1 小时鼻内给药)可显着减轻患有 ALI 的成年雄性 C57BL/6 小鼠的病理损伤并降低病理评分[2]。
动物实验
Animal/Disease Models: Female strain A/J mice at 8 weeks of age[3]
Doses: 2.0 mg/ kg
Route of Administration: Orally via their diet; at 2, 7 and 21 days prior to killing (27 weeks)
Experimental Results: decreased the size of the lung tumors after 2 days and rapidly diminished the size of lung tumors, reversed DNA hypomethylation and modulated mRNA expression of genes.
药代性质 (ADME/PK)
Absorption, Distribution and Excretion
Extended release oral capsules are 9-21% bioavailable. A 9mg dose reaches a Cmax of 1.50±0.79ng/mL with a Tmax of 2-8h and an AUC of 7.33ng\*hr/mL. A high fat meal increases the Tmax by 2.3h but otherwise does not affect the pharmacokinetics of budesonide. 180-360µg metered inhaled doses of budesonide are 34% deposited in the lungs, 39% bioavailable, and reach a Cmax of 0.6-1.6nmol/L with a Tmax of 10 minutes. A 1mg nebulized dose is 6% bioavailable, reaching a Cmax of 2.6nmol/L with a Tmax of 20 minutes. A 9mg oral extended release tablet reaches a Cmax of 1.35±0.96ng/mL with a Tmax of 13.3±5.9h and an AUC of 16.43±10.52ng\*hr/mL. Budesonide rectal foam 2mg twice daily has an AUC of 4.31ng\*hr/mL.
Approximately 60% of a budesonide dose is recovered in the urine as the major metabolites 6beta-hydroxybudesonide, 16alpha-hydroxyprednisolone, and their conjugates. No unchanged budesonide is recovered in urine.
The volume of distribution of budesonide is 2.2-3.9L/kg.
Budesonide has a plasma clearance of 0.9-1.8L/min. The 22R form has a clearance of 1.4L/min while the 22S form has a clearance of 1.0L/min. The clearance in asthmatic children 4-6 years old is 0.5L/min.
/MILK/ Not known whether budesonide is distributed in milk.
When budesonide is administered intranasally, approximately 34% of a dose reaches systemic circulation. Mean peak plasma budesonide concentrations are achieved in about 0.7 hours.
Inhaled corticosteroids (ICS) are mainstay treatment of asthma and chronic obstructive pulmonary disease. However, highly lipophilic ICS accumulate in systemic tissues, which may lead to adverse systemic effects. The accumulation of a new, highly lipophilic ICS, ciclesonide and its active metabolite (des-CIC) has not yet been reported. Here, we have compared tissue accumulation of des-CIC and an ICS of a moderate lipophilicity, budesonide (BUD), after 14 days of once-daily treatment in mice. Single, three or 14 daily doses of [(3) H]-des-CIC or [(3) H]-BUD were administered subcutaneously to male CD1 albino mice, which were killed at 4 hrs, 24 hrs or 5 days after the last dose. Distribution of tissue concentration of radioactivity was studied by quantitative whole-body autoradiography. Pattern of radioactivity distribution across most tissues was similar for both corticosteroids after a single as well as after repeated dosing. However, tissue concentration of radioactivity differed between des-CIC and BUD. After a single dose, concentrations of radioactivity for both corticosteroids were low for most tissues but increased over 14 days of daily dosing. The tissue radioactivity of des-CIC at 24 hrs and 5 days after the 14th dose was 2-3 times higher than that of BUD in majority of tissues. Tissue accumulation, assessed as concentration of tissue radioactivity 5 days after the 14th versus 3rd dose, showed an average ratio of 5.2 for des-CIC and 2.7 for BUD (p < 0.0001). In conclusion, des-CIC accumulated significantly more than BUD. Systemic accumulation may lead to increased risk of adverse systemic side effects during long-term therapy.
Metabolism / Metabolites
Budesonide is 80-90% metabolized at first pass. Budesonide is metabolized by CYP3A to its 2 major metabolites, 6beta-hydroxybudesonide and 16alpha-hydroxyprednisolone. The glucocorticoid activity of these metabolites is negligible (<1/100) in relation to that of the parent compound. CYP3A4 is the strongest metabolizer of budesonide, followed by CYP3A5, and CYP3A7.
Budesonide is metabolized in the liver by the cytochrome P-450 (CYP) isoenzyme 3A4; the 2 main metabolites have less than 1% of affinity for glucocorticoid receptors than the parent compound. Budesonide is excreted in urine and feces as metabolites.
Asthma is one of the most prevalent diseases in the world, for which the mainstay treatment has been inhaled glucocorticoids (GCs). Despite the widespread use of these drugs, approximately 30% of asthma sufferers exhibit some degree of steroid insensitivity or are refractory to inhaled GCs. One hypothesis to explain this phenomenon is interpatient variability in the clearance of these compounds. The objective of this research is to determine how metabolism of GCs by the CYP3A family of enzymes could affect their effectiveness in asthmatic patients. In this work, the metabolism of four frequently prescribed inhaled GCs, triamcinolone acetonide, flunisolide, budesonide, and fluticasone propionate, by the CYP3A family of enzymes was studied to identify differences in their rates of clearance and to identify their metabolites. Both interenzyme and interdrug variability in rates of metabolism and metabolic fate were observed. CYP3A4 was the most efficient metabolic catalyst for all the compounds, and CYP3A7 had the slowest rates. CYP3A5, which is particularly relevant to GC metabolism in the lungs, was also shown to efficiently metabolize triamcinolone acetonide, budesonide, and fluticasone propionate. In contrast, flunisolide was only metabolized via CYP3A4, with no significant turnover by CYP3A5 or CYP3A7. Common metabolites included 6 Beta-hydroxylation and Delta (6)-dehydrogenation for triamcinolone acetonide, budesonide, and flunisolide. The structure of Delta (6)-flunisolide was unambiguously established by NMR analysis. Metabolism also occurred on the D-ring substituents, including the 21-carboxy metabolites for triamcinolone acetonide and flunisolide. The novel metabolite 21-nortriamcinolone acetonide was also identified by liquid chromatography-mass spectrometry and NMR analysis.
Biological Half-Life
Budesonide has a plasma elimination half life of 2-3.6h. The terminal elimination half life in asthmatic children 4-6 years old is 2.3h.
毒性/毒理 (Toxicokinetics/TK)
Hepatotoxicity
Long term therapy with budesonide has not been linked to elevations in serum enzyme levels, and in clinical trials rates of ALT elevations were similar with budesonide as with placebo treatment. In controlled trials, there were no reported cases of clinically apparent liver injury associated with its use. Unlike conventional systemically administered corticosteroids, budesonide has not been linked to episodes of reactivation of hepatitis B. Budesonide has been used in severe autoimmune liver diseases without evidence that it causes worsening of liver injury. Because it can improve serum aminotransferase elevations in patients with autoimmune hepatitis, its withdrawal may be followed by rebound elevations as also occurs with conventional corticosteroid therapy. In addition, there has been a single case report of acute serum aminotransferase elevations during budesonide therapy that resolved when the drug was stopped, but documentation was limited and the patient was on multiple other potentially hepatotoxic drugs.
Likelihood score: E (unlikely cause of clinically apparent liver injury).
Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
The amounts of inhaled budesonide excreted into breastmilk are minute and infant exposure is negligible. When taken by mouth, budesonide is only about 9% bioavailable; bioavailability in the infant is likely to be similarly low for any budesonide that enters the breastmilk. Expert opinion considers inhaled, nasal, oral and rectal corticosteroids acceptable to use during breastfeeding.
◉ Effects in Breastfed Infants
None reported with any corticosteroid.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.
Protein Binding
Corticosteroids are generally bound to corticosteroid binding globulin and serum albumin in plasma. Budesonide is 85-90% protein bound in plasma.
参考文献

[1]. Transactivation via the Human Glucocorticoid and Mineralocorticoid Receptor by Therapeutically Used Steroids in CV-1 Cells: A Comparison of Their Glucocorticoid and Mineralocorticoid Properties. Eur J Endocrinol. 2004 Sep;151(3):397-406.

[2]. Intranasal Application of Budesonide Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Suppressing Nucleotide-Binding Oligomerization Domain-Like Receptor Family, Pyrin Domain-Containing 3 Inflammasome Activation in Mice. J Immunol Res. 2019 Feb 27;2019:7264383.

[3]. Modulation by Budesonide of DNA Methylation and mRNA Expression in Mouse Lung Tumors. Int J Cancer. 2007 Mar 1;120(5):1150-3.

其他信息
Budesonide is a glucocorticoid steroid having a highly oxygenated pregna-1,4-diene structure. It is used mainly in the treatment of asthma and non-infectious rhinitis and for treatment and prevention of nasal polyposis. It has a role as an anti-inflammatory drug, a bronchodilator agent and a drug allergen. It is an 11beta-hydroxy steroid, a glucocorticoid, a cyclic acetal, a 20-oxo steroid, a 21-hydroxy steroid, a 3-oxo-Delta(1),Delta(4)-steroid and a primary alpha-hydroxy ketone. It derives from a hydride of a pregnane.
Budesonide is a glucocorticoid that is a mix of the 22R and 22S epimer used to treat inflammatory conditions of the lungs and intestines such as asthma, COPD, Crohn's disease, and ulcerative colitis. Budesonide was granted FDA approval on 14 February 1994. It is also available in a combination product with [formoterol].
Budesonide is a Corticosteroid. The mechanism of action of budesonide is as a Corticosteroid Hormone Receptor Agonist.
Budesonide is a corticosteroid that undergoes high first pass elimination by the liver so that systemic levels after oral administration are minimal. Budesonide has been used orally for several immune mediated gastrointestinal and liver diseases and as nasal spray or by inhalation for allergic rhinitis, asthma and chronic obstructive lung disease. Neither inhalant nor oral budesonide has been linked to serum enzyme elevations during therapy or to convincing instances of clinically apparent acute liver injury.
Budesonide is a synthetic glucocorticoid with anti-inflammatory and immunomodulating properties. Upon administration, budesonide binds to intracellular glucocorticoid receptors (GRs) and induces the expression of glucocorticoid-responsive genes that encode for anti-inflammatory mediators, such as certain anti-inflammatory cytokines, including interleukin 10 (IL-10), and lipocortins. Lipocortins inhibit phospholipase A2, thereby blocking the release of arachidonic acid from membrane phospholipids and preventing the synthesis of prostaglandins and leukotrienes, both mediators of inflammation. In addition, budesonide prevents the release of pro-inflammatory cytokines from epithelial cells and macrophages, including interleukin 6 (IL-6), IL-8, interferon-beta (IFNb), and inhibits nuclear factor kappa-B (NF-kB) activation thereby decreasing NF-kB-mediated inflammation.
A glucocorticoid used in the management of ASTHMA, the treatment of various skin disorders, and allergic RHINITIS.
See also: Albuterol sulfate; budesonide (component of); Budesonide; formoterol fumarate dihydrate (component of); Budesonide; formoterol fumarate; glycopyrrolate (component of) ... View More ...
Drug Indication
Budesonide extended-release capsules are indicated for the treatment and maintenance of mild to moderate Crohn’s disease. Various inhaled budesonide products are indicated for prophylactic therapy in asthma and to reduce exacerbations of COPD. A budesonide nasal spray is available over the counter for symptoms of hay fever and upper respiratory allergies. Extended-release capsules are indicated to induce remission of mild to moderate ulcerative colitis and a rectal foam is used for mild to moderate distal ulcerative colitis. In addition, a delayed-release capsule formulation of budesonide is indicated to reduce proteinuria in adults with IgA nephropathy at risk of rapid disease progression. Budesonide is indicated to treat eosinophilic esophagitis (EoE): For this indication, it is only approved for use in adults in Europe while it is approved for short-term use (12 weeks) in patients 11 years of age and older in the US.
FDA Label
Kinpeygo is indicated for the treatment of primary immunoglobulin A (IgA) nephropathy (IgAN) in adults at risk of rapid disease progression with a urine protein-to-creatinine ratio (UPCR) ≥1. 5 g/gram.
Jorveza is indicated for the treatment of eosinophilic esophagitis (EoE) in adults (older than 18 years of age).
Treatment of primary IgA nephropathy
Treatment of asthma
Prevention of bronchopulmonary dysplasia
Mechanism of Action
The short term effects of corticosteroids are decreased vasodilation and permeability of capillaries, as well as decreased leukocyte migration to sites of inflammation. Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days. Glucocorticoids inhibit neutrophil apoptosis and demargination; they inhibit phospholipase A2, which decreases the formation of arachidonic acid derivatives; they inhibit NF-Kappa B and other inflammatory transcription factors; they promote anti-inflammatory genes like interleukin-10. Lower doses of corticosteroids provide an anti-inflammatory effect, while higher doses are immunosuppressive. High doses of glucocorticoids for an extended period bind to the mineralocorticoid receptor, raising sodium levels and decreasing potassium levels.
To investigate the roles of signal transduction and activator of transcription 6 (STAT6) and orosomucoid 1-like 3 (ORMDL3) in airway remodeling among asthmatic mice and to observe the effects of budesonide (BUD) on their expression, thirty mice were randomly divided into control, asthma, and BUD intervention group. The mice were sensitized and challenged with ovalbumin (OVA) to establish a mouse model of asthma. The BUD intervention group received aerosol inhalation of BUD dissolved in normal saline 30 minutes before each OVA challenge, while normal saline was used instead of OVA solution in the control group. The pathological changes in the airway were observed by hematoxylin-eosin staining and Masson staining. The interleukin-13 (IL-13) level in lung homogenate was measured by enzyme-linked immunosorbent assay. The mRNA expression of STAT6 and ORMDL3 was measured by RT-PCR. The asthma group showed more pathological changes in the airway than the control and BUD intervention groups, and the BUD intervention group had reduced pathological changes in the airway compared with the asthma group. The asthma and BUD intervention groups had significantly higher IL-13 levels and mRNA expression of STAT6 and ORMDL3 than the control group (P<0.05), and these indices were significantly higher in the asthma group than in the BUD intervention group (P<0.05). The Pearson correlation analysis showed that STAT6 mRNA expression was positively correlated with ORMDL3 mRNA expression (r=0.676, P=0.032). STAT6 and ORMDL3 may be involved in the airway remodeling of mice, and BUD can reduce airway remodeling in asthmatic mice, possibly by down-regulating mRNA expression of STAT6 and ORMDL3.
Mucus hypersecretion from airway epithelium is a characteristic feature of severe asthma. Glucocorticoids (GCs) may suppress mucus production and diminish the harmful airway obstruction. We investigated the ability of GCs to suppress mRNA expression and protein synthesis of a gene encoding mucin, MUC5AC, induced by transforming growth factor (TGF)-alpha in human mucoepidermoid carcinoma (NCI-H292) cells and the molecular mechanisms underlying the suppression. We determined if GCs such as dexamethasone (DEX), budesonide (BUD), and fluticasone (FP) could suppress MUC5AC production induced by a combination of TGF-alpha and double-strand RNA, polyinosinic-polycytidylic acid (polyI:C). MUC5AC mRNA expression and MUC5AC protein production were evaluated. The signaling pathways activated by TGF-alpha and their inhibition by GCs were tested using a phosphoprotein assay and MUC5AC promoter assay. DEX significantly suppressed the expression of MUC5AC mRNA and MUC5AC protein induced by TGF-alpha. The activation of the MUC5AC promoter by TGF-alpha was significantly inhibited by DEX. DEX did not affect activation of downstream pathways of the EGF receptor or mRNA stability of MUC5AC transcripts. DEX, BUD, and FP suppressed MUC5AC protein expression induced by a combination of TGF-alpha and polyI:C in a dose-dependent manner. GCs inhibited MUC5AC production induced by TGF-alpha alone or a combination of TGF-alpha and polyI:C; the repression may be mediated at the transcriptional but not post-transcriptional level.
*注: 文献方法仅供参考, InvivoChem并未独立验证这些方法的准确性
化学信息 & 存储运输条件
分子式
C25H34O6
分子量
430.53
精确质量
430.235
CAS号
51333-22-3
相关CAS号
Budesonide-d8;1105542-94-6;Budesonide (Standard);51333-22-3
PubChem CID
5281004
外观&性状
White to off-white solid powder
密度
1.3±0.1 g/cm3
沸点
599.7±50.0 °C at 760 mmHg
熔点
221-232ºC (dec.)
闪点
201.8±23.6 °C
蒸汽压
0.0±3.9 mmHg at 25°C
折射率
1.592
LogP
3.14
tPSA
93.06
氢键供体(HBD)数目
2
氢键受体(HBA)数目
6
可旋转键数目(RBC)
4
重原子数目
31
分子复杂度/Complexity
862
定义原子立体中心数目
8
SMILES
CCCC1O[C@@H]2C[C@H]3[C@@H]4CCC5=CC(=O)C=C[C@@]5([C@H]4[C@H](C[C@@]3([C@@]2(O1)C(=O)CO)C)O)C
InChi Key
VOVIALXJUBGFJZ-KWVAZRHASA-N
InChi Code
InChI=1S/C25H34O6/c1-4-5-21-30-20-11-17-16-7-6-14-10-15(27)8-9-23(14,2)22(16)18(28)12-24(17,3)25(20,31-21)19(29)13-26/h8-10,16-18,20-22,26,28H,4-7,11-13H2,1-3H3/t16-,17-,18-,20+,21?,22+,23-,24-,25+/m0/s1
化学名
(6aR,6bS,7S,8aS,8bS,11aR,12aS,12bS)-7-hydroxy-8b-(2-hydroxyacetyl)-6a,8a-dimethyl-10-propyl-6a,6b,7,8,8a,8b,11a,12,12a,12b-decahydro-1H-naphtho[2,1:4,5] indeno[1,2-d][1,3]dioxol-4(2H)-one
别名

Rhinocort; Budicort; Entocort;Rhinosol; Pulmicort; Symbicort; Noex Entocort EC

HS Tariff Code
2934.99.9001
存储方式

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

运输条件
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
溶解度数据
溶解度 (体外实验)
DMSO: 86 mg/mL (199.7 mM)
Water:<1 mg/mL
Ethanol: 19 mg/mL (44.1 mM)
溶解度 (体内实验)
配方 1 中的溶解度: ≥ 2.08 mg/mL (4.83 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加,逐一添加), 澄清溶液。
例如,若需制备1 mL的工作液,可将100 μL 20.8 mg/mL澄清DMSO储备液加入400 μL PEG300中,混匀;然后向上述溶液中加入50 μL Tween-80,混匀;加入450 μL生理盐水定容至1 mL。
*生理盐水的制备:将 0.9 g 氯化钠溶解在 100 mL ddH₂O中,得到澄清溶液。

配方 2 中的溶解度: ≥ 2.08 mg/mL (4.83 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加,逐一添加), 澄清溶液。
例如,若需制备1 mL的工作液,可将 100 μL 20.8 mg/mL澄清DMSO储备液加入900 μL 20% SBE-β-CD生理盐水溶液中,混匀。
*20% SBE-β-CD 生理盐水溶液的制备(4°C,1 周):将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中,得到澄清溶液。

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配方 3 中的溶解度: ≥ 2.08 mg/mL (4.83 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加,逐一添加), 澄清溶液。
例如,若需制备1 mL的工作液,可将 100 μL 20.8 mg/mL 澄清 DMSO 储备液加入到 900 μL 玉米油中并混合均匀。


请根据您的实验动物和给药方式选择适当的溶解配方/方案:
1、请先配制澄清的储备液(如:用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液,按从左到右的顺序依次添加助溶剂,澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明,并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中,混合均匀/澄清;向上述体系中加入50 μL Tween-80,混合均匀/澄清;然后继续加入450 μL ddH2O (或 saline)定容至 1 mL;

3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出,可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果,工作液请现配现用!
6、如不确定怎么将母液配置成体内动物实验的工作液,请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。
制备储备液 1 mg 5 mg 10 mg
1 mM 2.3227 mL 11.6136 mL 23.2272 mL
5 mM 0.4645 mL 2.3227 mL 4.6454 mL
10 mM 0.2323 mL 1.1614 mL 2.3227 mL

1、根据实验需要选择合适的溶剂配制储备液 (母液):对于大多数产品,InvivoChem推荐用DMSO配置母液 (比如:5、10、20mM或者10、20、50 mg/mL浓度),个别水溶性高的产品可直接溶于水。产品在DMSO 、水或其他溶剂中的具体溶解度详见上”溶解度 (体外)”部分;

2、如果您找不到您想要的溶解度信息,或者很难将产品溶解在溶液中,请联系我们;

3、建议使用下列计算器进行相关计算(摩尔浓度计算器、稀释计算器、分子量计算器、重组计算器等);

4、母液配好之后,将其分装到常规用量,并储存在-20°C或-80°C,尽量减少反复冻融循环。

计算器

摩尔浓度计算器可计算特定溶液所需的质量、体积/浓度,具体如下:

  • 计算制备已知体积和浓度的溶液所需的化合物的质量
  • 计算将已知质量的化合物溶解到所需浓度所需的溶液体积
  • 计算特定体积中已知质量的化合物产生的溶液的浓度
使用摩尔浓度计算器计算摩尔浓度的示例如下所示:
假如化合物的分子量为350.26 g/mol,在5mL DMSO中制备10mM储备液所需的化合物的质量是多少?
  • 在分子量(MW)框中输入350.26
  • 在“浓度”框中输入10,然后选择正确的单位(mM)
  • 在“体积”框中输入5,然后选择正确的单位(mL)
  • 单击“计算”按钮
  • 答案17.513 mg出现在“质量”框中。以类似的方式,您可以计算体积和浓度。

稀释计算器可计算如何稀释已知浓度的储备液。例如,可以输入C1、C2和V2来计算V1,具体如下:

制备25毫升25μM溶液需要多少体积的10 mM储备溶液?
使用方程式C1V1=C2V2,其中C1=10mM,C2=25μM,V2=25 ml,V1未知:
  • 在C1框中输入10,然后选择正确的单位(mM)
  • 在C2框中输入25,然后选择正确的单位(μM)
  • 在V2框中输入25,然后选择正确的单位(mL)
  • 单击“计算”按钮
  • 答案62.5μL(0.1 ml)出现在V1框中
g/mol

分子量计算器可计算化合物的分子量 (摩尔质量)和元素组成,具体如下:

注:化学分子式大小写敏感:C12H18N3O4  c12h18n3o4
计算化合物摩尔质量(分子量)的说明:
  • 要计算化合物的分子量 (摩尔质量),请输入化学/分子式,然后单击“计算”按钮。
分子质量、分子量、摩尔质量和摩尔量的定义:
  • 分子质量(或分子量)是一种物质的一个分子的质量,用统一的原子质量单位(u)表示。(1u等于碳-12中一个原子质量的1/12)
  • 摩尔质量(摩尔重量)是一摩尔物质的质量,以g/mol表示。
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配液计算器可计算将特定质量的产品配成特定浓度所需的溶剂体积 (配液体积)

  • 输入试剂的质量、所需的配液浓度以及正确的单位
  • 单击“计算”按钮
  • 答案显示在体积框中
动物体内实验配方计算器(澄清溶液)
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)
第二步:请输入动物体内配方组成(配方适用于不溶/难溶于水的化合物),不同的产品和批次配方组成不同,如对配方有疑问,可先联系我们提供正确的体内实验配方。此外,请注意这只是一个配方计算器,而不是特定产品的确切配方。
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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)。如该浓度超过该批次药物DMSO溶解度,请首先与我们联系。

体内配方配制方法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 ddH2O,混匀澄清。

(1) 请确保溶液澄清之后,再加入下一种溶剂 (助溶剂) 。可利用涡旋、超声或水浴加热等方法助溶;
            (2) 一定要按顺序加入溶剂 (助溶剂) 。

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