在 L929 细胞中，倍他米松（0.1–1 μM；12 小时）可增加基因表达[4]。 CEM C7 T 细胞凋亡由倍他米松（0.1–1 μM；48 小时）诱导[4]。

由于倍他米松（0.48 mg；IVGT 48 小时）可减少脑血管舒张，因此可减轻高碳酸血症引起的 CBF 增加[1]。局部给予倍他米松 (0.05 ml; 1 mg/L) 会降低大鼠脑中 NF-κB 的活化，升高 TNFα 和 IL-1β，并刺激 IL-10 的表达，所有这些都是由机械性异常性疼痛和热引起的脊髓神经横断引起的痛觉过敏[2]。

Animal/Disease Models: Rambouillet-Colombia ewes bred on a single occasion are received hypercapnic challenges[1]
Doses: 0.48 mg
Route of Administration: Injected into the fetal jugular vein at a rate of 1 ml/h (10 μg betamethasone/h) and maintained over the next 48 h.
Experimental Results: diminished cerebral blood flow (CBF) in all brain regions measured except the hippocampus after 24 h of infusion. The reduction in CBF was diminished to about 25-30 % after 48 h of infusion.

Absorption, Distribution and Excretion
The absorption and potency of any topical corticosteroid including betamethasone depends on the vehicle in which the steroid is delivered. For example, betamethasone dipropionate 0.05% ointment is classified as a highly potent topical steroid, while betamethasone dipropionate 0.05% cream or lotion is considered to be moderately potent. There are several structural modifications that can determine the potency of a topical corticosteroid. For example, corticosteroids containing a halogen at specific carbons, or that contain esters are more potent due to enhanced lipophilicity. As such, there is a marked difference between topical products containing betamethasone dipropionate vs. betamethasone valerate. Betamethasone dipropionate contains 2 esters which enhances its potency, while betamethasone valerate has only one ester and is less potent. It should be noted that the use of occlusive dressings with topical steroids significantly increases the absorption, increasing the risk for adverse effects.
Corticosteroids are eliminated predominantly in the urine.
In a study that included Indian women of reproductive age, the volume of distribution following a single intramuscular dose of betamethasone phosphate was 94,584±23,539 mL(s).
In a study that included Indian women of reproductive age, the CL/F following a single intramuscular dose of betamethasone phosphate was 6,466 ± 805 mL/hour.
Glucocorticoids ... absorbed systemically from sites of local administration, such as synovial spaces, the conjunctival sac, skin, and respiratory tract. When administration is prolonged, when the site of application is covered with an occlusive dressing, or when large areas of skin are involved, the absorption may be sufficient to cause systemic effects, including suppression of the HPA axis. /Adrenocorticalsteroids/
Following absorption, 90% or more of cortisol in plasma is reversibly bound to protein under normal circumstances. Only the fraction of corticosteroid that is unbound can enter cells to mediate corticosteroid effects. Two plasma proteins account for almost all of the steroid-binding capacity: corticosteroid-binding globulin (CBG; also called transcortin), and albumin. CBG is an alpha-globulin secreted by the liver that has high affinity for steroids but relatively low total binding capacity, whereas albumin, also produced by the liver, has low affinity but relatively large binding capacity. At normal or low concentrations of corticosteroids, most of the hormone is protein-bound. At higher steroid concentrations, the capacity of protein binding is exceeded, and a significantly greater fraction of the steroid exists in the free state. Corticosteroids compete with each other for binding sites on CBG. CBG has relatively high affinity for cortisol and most of its synthetic congeners and low affinity for aldosterone and glucuronide-conjugated steroid metabolites; thus, greater percentages of these latter steroids are found in the free form. /Adrenocortical Steroids/
The pharmacokinetics of betamethasone and its phosphate ester are described in 8 healthy adults after iv bolus injection of 10.6 mg betamethasone phosphate. Both cmpd were measured by high performance liquid chromatography with ultraviolet detection using sample handling methods which prevented hydrolysis of the ester in vitro. Betamethasone phosphate disappeared rapidly from plasma (mean half-life = 4.7 min) as betamethasone levels rose. Betamethasone plasma levels reached a peak 10-36 min after admin of the phosphate before declining in a biexponential manner. The terminal slow disposition phase had a mean half-life of 6.5 hr. Only about 5% of the dose was recovered from urine as betamethasone, indicating extensive extrarenal clearance of betamethasone. /Betamethason phosphate/

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Metabolism / Metabolites
The metabolism of betamethasone yields 6 metabolites. The metabolic processes include 6β hydroxylation, 11β-hydroxyl oxidation, and reduction of the C-20 carbonyl group followed by removal of the side chain.
All of the biologically active adrenocortical steroids and their synthetic congeners have a double bond in the 4,5 position and a ketone group at C 3. As a general rule, the metabolism of steroid hormones involves sequential additions of oxygen or hydrogen atoms, followed by conjugation to form water-soluble derivatives. Reduction of the 4,5 double bond occurs at both hepatic and extrahepatic sites, yielding inactive compounds. Subsequent reduction of the 3-ketone substituent to the 3-hydroxyl derivative, forming tetrahydrocortisol, occurs only in the liver. Most of these A ring-reduced steroids are conjugated through the 3-hydroxyl group with sulfate or glucuronide by enzymatic reactions that take place in the liver and, to a lesser extent, in the kidney. The resultant sulfate esters and glucuronides form water-soluble derivatives and are the predominant forms excreted in the urine. Neither biliary nor fecal excretion is of quantitative importance in human beings. /Adrenocortical Steroids/

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Biological Half-Life
In a study that included Indian women of reproductive age, the half-life following a single intramuscular dose of betamethasone phosphate was 10.2 ± 2.5 hours.
The pharmacokinetics of betamethasone and its phosphate ester are described in 8 healthy adults after i.v. bolus injection of 10.6 mg betamethasone phosphate. Both compounds were measured by high-performance liquid chromatography with ultraviolet detection using sample handling methods which prevented hydrolysis of the ester in vitro. Betamethasone phosphate disappeared rapidly from plasma (mean half-life = 4.7 min) as betamethasone levels rose. Betamethasone plasma levels reached a peak 10-36 min after administration of the phosphate before declining in a biexponential manner. The terminal slow disposition phase had a mean half-life of 6.5 hr.
Serum half-life of betamethasone is about 3 hr.

Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Since only extensive application of the most potent corticosteroids may cause systemic effects in the mother, it is unlikely that short-term application of topical corticosteroids would pose a risk to the breastfed infant by passage into breastmilk. However, it would be prudent to use the least potent drug on the smallest area of skin possible. It is particularly important to ensure that the infant's skin does not come into direct contact with the areas of skin that have been treated. Only the lower potency corticosteroids should be used on the nipple or areola where the infant could directly ingest the drugs from the skin; topical betamethasone should be avoided on the nipple. Betamethasone ointment appears to have no advantage over lanolin for treating sore nipples during breastfeeding. Current guidelines allow topical corticosteroids to be applied to the nipples just after nursing for eczema, with the nipples cleaned gently before nursing. Only water-miscible cream or gel products should be applied to the breast or nipple because ointments may expose the infant to high levels of mineral paraffins via licking.
◉ Effects in Breastfed Infants
Topical application of a corticosteroid with relatively high mineralocorticoid activity (isofluprednone acetate) to the mother's nipples resulted in prolonged QT interval, cushingoid appearance, severe hypertension, decreased growth and electrolyte abnormalities in her 2-month-old breastfed infant. The mother had used the cream since birth for painful nipples.
A woman who was nursing (extent not stated) her newborn infant was treated for pemphigus with oral prednisolone 25 mg daily, with the dosage increased over 2 weeks to 60 mg daily. She was also taking cetirizine 10 mg daily and topical betamethasone 0.1% twice daily to the lesions. Because of a poor response, the betamethasone was changed to clobetasol propionate ointment 0.05%. She continued breastfeeding throughout treatment and her infant was developing normally at 8 weeks of age and beyond.
◉ Effects on Lactation and Breastmilk
In a randomized, double-bind trial, lanolin was compared to an all-purpose nipple ointment containing betamethasone 0.05%, mupirocin 1%, and miconazole 2% for painful nipples while nursing in the first 2 weeks postpartum. The two treatments were equally effective in reducing nipple pain, nipple healing time, breastfeeding duration, breastfeeding exclusivity rate, mastitis and nipple symptoms, side effects or maternal satisfaction with treatment.
◉ Summary of Use during Lactation
Betamethasone has not been well studied during breastfeeding. Systemic betamethasone is best avoided in favor of one of the shorter-acting and better studied alternatives because of its potency and low protein binding which would favor its passage into milk. Use of betamethasone 3 to 9 days prior to delivery of a preterm infant might decrease postpartum milk production in some women. Local injections, such as for tendinitis, would not be expected to cause any adverse effects in breastfed infants, but might occasionally cause temporary loss of milk supply. See also Betamethasone, Topical.
◉ Effects in Breastfed Infants
None reported with any corticosteroid.
◉ Effects on Lactation and Breastmilk
A 5.7 mg dose of depot betamethasone injected into the shoulder for bursitis had no effect in the milk supply in one mother. However, medium to large doses of depot corticosteroids injected into joints have been reported to cause temporary reduction of lactation.
A double-blind study in the 1970s randomized pregnant women in preterm labor to either 6 mg of short-acting betamethasone phosphate plus 6 mg long-acting betamethasone acetate or a control treatment containing 6 mg cortisone acetate. Later in the trial, the doses were doubled because of an incomplete response. A total of 560 women received betamethasone and 582 received cortisone. No difference was seen in the percentage of women lactating at hospital discharge (32% and 30.5%, respectively); however, these percentages are very low compared to the rates in many hospitals today.
A study of 46 women who delivered an infant before 34 weeks of gestation found that a course of betamethasone (2 intramuscular injections of 11.4 mg of betamethasone 24 hours apart) given between 3 and 9 days before delivery resulted in delayed lactogenesis II and lower average milk volumes during the 10 days after delivery. Milk volume was not affected if the infant was delivered less than 3 days or more than 10 days after the mother received the corticosteroid.
A study of 87 pregnant women found that betamethasone given as above during pregnancy caused a premature stimulation of lactose secretion during pregnancy. Although the increase was statistically significant, the clinical importance appears to be minimal.

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Protein Binding
Betamethasone valerate binds to serum albumin and corticosteroid-binding globulin.

[1]. Effects of betamethasone administration to the fetal sheep in late gestation on fetal cerebral blood flow. J Physiol. 2000 Nov 1;528(Pt 3):619-32.

[2]. Betamethasone affects cerebral expressions of NF-kappaB and cytokines that correlate with pain behavior in a rat model of neuropathy. Ann Clin Lab Sci. Winter 2006;36(1):39-46.

[3]. Clinical Efficiency of Topical Calcipotriol/Betamethasone Treatment in Psoriasis Relies on Suppression of the Inflammatory TNFα - IL-23 - IL-17 Axis. Acta Derm Venereol. 2017 Apr 6;97(4):449-455.

[4]. Various glucocorticoids differ in their ability to induce gene expression, apoptosis and to repress NF-kappaB-dependent transcription. FEBS Lett. 1998 Dec 28;441(3):441-6.

Betamethasone is a glucocorticoid, a 20-oxo steroid, a 21-hydroxy steroid, a 17alpha-hydroxy steroid, a fluorinated steroid, an 11beta-hydroxy steroid, a 3-oxo-Delta(1),Delta(4)-steroid, a primary alpha-hydroxy ketone and a tertiary alpha-hydroxy ketone. It has a role as an anti-inflammatory drug, an anti-asthmatic agent and an immunosuppressive agent. It derives from a hydride of a pregnane.
Betamethasone is a long-acting corticosteroid with immunosuppressive and antiinflammatory properties. It can be used topically to manage inflammatory skin conditions such as eczema, and parenterally to manage several disease states including autoimmune disorders. Betamethasone has potent glucocorticoid activity and negligible mineralocorticoid activity.
Betamethasone is a Corticosteroid. The mechanism of action of betamethasone is as a Corticosteroid Hormone Receptor Agonist.
Betamethasone is a synthetic glucocorticoid with metabolic, immunosuppressive and anti-inflammatory activities. Betamethasone binds to specific intracellular glucocorticoid receptors and subsequently binds to DNA to modify gene expression. The synthesis of certain anti-inflammatory proteins is induced while the synthesis of certain inflammatory mediators is inhibited. As a result, there is an overall reduction in chronic inflammation and autoimmune reactions.
A glucocorticoid given orally, parenterally, by local injection, by inhalation, or applied topically in the management of various disorders in which corticosteroids are indicated. Its lack of mineralocorticoid properties makes betamethasone particularly suitable for treating cerebral edema and congenital adrenal hyperplasia. (From Martindale, The Extra Pharmacopoeia, 30th ed, p724)
See also: Betamethasone Valerate (active moiety of); Betamethasone Acetate (is active moiety of); Betamethasone Dipropionate (active moiety of) ... View More ...

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Drug Indication
As a member of the corticosteroid family, betamethasone is indicated for the treatment of several inflammatory conditions. As topical monotherapy, betamethasone is indicated to relieve pruritic and inflammatory symptoms of corticosteroid-responsive-dermatoses. Betamethasone can be used topically in combination with a vitamin D analog such as calcipotriene to treat plaque psoriasis. The corticosteroid is also available as an injectable suspension and can be used to manage a range of inflammatory conditions including endocrine disorders, gastrointestinal disorders, and rheumatic disorders among other conditions.
FDA Label

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Mechanism of Action
Glucocorticoids inhibit neutrophil apoptosis and demargination, and inhibit NF-Kappa B and other inflammatory transcription factors. They also inhibit phospholipase A2, leading to decreased formation of arachidonic acid derivatives. In addition, glucocorticoids promote anti-inflammatory genes like interleukin-10. Corticosteroids like betamethasone can act through nongenomic and genomic pathways. The genomic pathway is slower and occurs when glucocorticoids activate glucocorticoid receptors and initiate downstream effects that promote transcription of anti-inflammatory genes including phosphoenolpyruvate carboxykinase (PEPCK), IL-1-receptor antagonist, and tyrosine amino transferase (TAT). On the other hand, the nongenomic pathway is able to elicit a quicker response by modulating T-cell, platelet and monocyte activity through the use of existing membrane-bound receptors and second messengers.
Corticosteroids interact with specific receptor proteins in target tissues to regulate the expression of corticosteroid responsive genes, thereby changing the levels and array of proteins synthesized by the various target tissues. As a consequence of the time required for changes in gene expression and protein synthesis, most effects of corticosteroids are not immediate, but become apparent after several hours. ... Although corticosteroids predominantly act to increase expression of target genes, there are well documented examples where glucocorticoids decrease transcription of target genes ... In contrast to these genomic effects, recent studies have raised the possibility that some actions of corticosteroids are immediate and are mediated by membrane-bound receptors. /Adrenocorticosteroids/
The mechanisms by which glucocorticoids inhibit glucose utilization in peripheral tissues are not fully understood. Glucocorticoids decrease glucose uptake in adipose tissue, skin, fibroblasts, thymocytes, and polymorphonuclear leukocytes; these effects are postulated to result from translocation of the glucose transporters from the plasma membrane to an intracellular location. These peripheral effects are associated with a number of catabolic actions, including atrophy of lymphoid tissue, decreased muscle mass, negative nitrogen balance, and thinning of the skin. /Adrenocorticalsteroids/
The mechanisms by which the glucocorticoids promote gluconeogenesis are not fully defined. Amino acids mobilized from a number of tissues in response to glucocorticoids reach the liver and provide substrate for the production of glucose and glycogen. In the liver, glucocorticoids induce the transcription of a number of enzymes involved in gluconeogenesis and amino acid metabolism, including phosphoenolpyruvate carboxykinase, glucose-6-phosphatase, and fructose-2,6-bisphosphatase. Analyses of the molecular basis for regulation of phosphoenolpyruvate carboxykinase gene expression have identified complex regulatory influences involving an interplay among glucocorticoids, insulin, glucagon, and catecholamine. The effects of these hormones and amines on phosphoenolpyruvate carboxykinase gene expression mirror the complex regulation of gluconeogenesis in the intact organism. /Adrenocorticalsteroids/
... /A/ major action of corticosteroids on the cardiovascular system is to enhance vascular reactivity to other vasoactive substances. Hypoadrenalism generally is associated with hypotension and reduced response to vasoconstrictors such as norepinephrine and angiotensin II. This diminished pressor response is explained partly by recent studies in experimental systems showing that glucocorticoids increase expression of adrenergic receptors in the vascular wall. Conversely, hypertension is seen in patients with excessive glucocorticoid secretion, occurring in most patients with Cushing's syndrome and in a subset of patients treated with synthetic glucocorticoids (even those lacking any significant mineralocorticoid action). /Adrenocorticosteroids/
For more Mechanism of Action (Complete) data for BETAMETHASONE (8 total), please visit the HSDB record page.

C22H29FO5

392.46

392.199

378-44-9

Betamethasone disodium phosphate;151-73-5;Betamethasone-d5;Betamethasone dipropionate;5593-20-4;Betamethasone valerate;2152-44-5;Betamethasone hydrochloride;956901-32-9;Betamethasone acetate;987-24-6;Betamethasone-d5-1;2244574-92-1

9782

White to off-white solid powder

1.3±0.1 g/cm3

568.2±50.0 °C at 760 mmHg

235-237°C

297.5±30.1 °C

0.0±3.5 mmHg at 25°C

1.592

1.87

94.83

3

6

2

28

805

8

C[C@H]1C[C@H]2[C@@H]3CCC4=CC(=O)C=C[C@@]4([C@]3([C@H](C[C@@]2([C@]1(C(=O)CO)O)C)O)F)C

UREBDLICKHMUKA-DVTGEIKXSA-N

InChI=1S/C22H29FO5/c1-12-8-16-15-5-4-13-9-14(25)6-7-19(13,2)21(15,23)17(26)10-20(16,3)22(12,28)18(27)11-24/h6-7,9,12,15-17,24,26,28H,4-5,8,10-11H2,1-3H3/t12-,15-,16-,17-,19-,20-,21-,22-/m0/s1

(8S,9R,10S,11S,13S,14S,16S,17R)-9-fluoro-11,17-dihydroxy-17-(2-hydroxyacetyl)-10,13,16-trimethyl-6,7,8,11,12,14,15,16-octahydrocyclopenta[a]phenanthren-3-one

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: This product requires protection from light (avoid light exposure) during transportation and storage.

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

配方 1 中的溶解度: ≥ 2.5 mg/mL (6.37 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 25.0 mg/mL澄清DMSO储备液加入到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。

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配方 2 中的溶解度: ≥ 2.5 mg/mL (6.37 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 25.0 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: ≥ 2.5 mg/mL (6.37 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 25.0 mg/mL 澄清 DMSO 储备液加入到 900 μL 玉米油中并混合均匀。

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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;
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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。