GSK-3β (IC50 = 2.0 μM)

Cromoglycate sodium (Cromolyn disodium; FPL-670) is a chromone compound that operates by blocking the release of chemical mediators from sensitized mast cells. It is used for the preventive treatment of allergy and exercise-induced asthma but does not affect established asthma episodes.

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Cromolyn sodium was originally characterised as a mast cell stabiliser (Hoag 1991). However, it also inhibits neutrophil activation (Kay 1987), neutrophil chemotaxis (Bruijnzeel 1989), macrophage activation, tachykinin action, eicosanoid and cytokine release, and adhesion molecule expression (Yazid 2009). A more recent in vitro study (Yazid 2009) showed that Cromolyn sodium stimulates the anti‐inflammatory intracellular protein annexin‐A1 trafficking and release. Cromolyn sodium inhibits eicosanoid release due to inhibition of a phosphatase PP2A (phosphoprotein phosphatase; EC 3.1.3.16), which probably forms part of a control loop to limit annexin‐A1 release [3].

There were no alterations in ET-1 levels, damage scores, or inflammation in IIR mice treated with cromoglycate sodium (cromoglycate disodium; FPL-670) prior to ischemia (P>0.05, PreCr group vs. M group). In conclusion, by downregulating ET-1 and preventing persistent MC activation, the injection of Cromolyn (sodium) after reperfusion, but not before ischemia, attenuates IIRI [1]. The action of Cromolyn (sodium) is to prevent chronic lung disease (CLD). It is not advised to use cromolyn (sodium) to protect premature newborns from developing chronic lung illness [2].

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Stabilizing mast cells (MCs) can either inhibit or augment inflammation; however, how improved therapeutic benefits against small intestinal ischemia-reperfusion injury (IIRI) can be achieved by stabilizing MCs remains to be elucidated. The present study was designed to evaluate different treatments with Cromolyn sodium (CS, an MC stabilizer), which was administrated either prior to ischemia or after reperfusion. Kunming mice were randomized into a sham-operated group (SH), a sole IIR group (M), in which mice were subjected to 30 min superior mesenteric artery occlusion followed by 3 day or 3 h reperfusion, or IIR, treated with CS 15 min prior to ischemia or 15 min after reperfusion in the PreCr and PostCr groups. The survival rate and Chiu's scores were evaluated. The levels of ET-1, histamine, TNF-α and IL-6, and expression of MC protease 7 (MCP7), MC counts and myeloperoxidase (MPO) activity were quantified. IIR resulted in severe injury as demonstrated by significant increases in mortality and injury score. IIR also led to substantial elevations in the levels of ET-1, histamine, TNF-α and IL-6, expression of MCP7, MC counts and MPO activities (P<0.05, M vs. SH groups). All biochemical changes were markedly reduced in the PostCr group (P<0.05, PostCr vs. M groups), whereas pretreatment of IIR mice with CS prior to ischemia exhibited no changes of ET-1 levels, injury score and inflammation (P>0.05, PreCr vs. M groups). In conclusion, administration of CS after reperfusion, but not prior to ischemia, attenuates IIRI by downregulating ET-1 and suppressing sustained MC activation. [1]

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Cromolyn, tranilast and cetirizine ameliorate SIN-triggered local HRARs [2]
As SIN-triggered HRARs are mainly mediated by histamine release, we examined whether clinically available mast cell stabilizers and histamine receptor blockers could prevent SIN-induced HRARs. Hence, cromolyn, tranilast and cetirizine were employed in the experiments. The results demonstrated that cromolyn, tranilast and cetirizine significantly decreased the amount of Evans blue dye in the skin of SIN-treated animals (Fig. 4A and B) alongside with reduction of SIN-induced increase of mast cell numbers (Fig. 4C and D). Considering the critical role of IL-33 in SIN-triggered HRARs, we determined whether inhibition of IL-33 production contributed to the ameliorative effect of these three agents in the PCA model. Immunohistochemistry analysis revealed that cromolyn, tranilast and cetirizine inhibited SIN-induced IL-33 production in the skin of PCA rats (Fig. 4E), which is consistent with previous reports

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Cromolyn, tranilast and cetirizine block SIN-triggered systemic HRARs [2]
We further validated the effect of these mast cell stabilizers on the prevention of SIN-triggered systemic HRARs in rats, and the results demonstrated that cromolyn, tranilast and cetirizine could effectively reverse SIN-induced body temperature reductions, and animals treated with 200 mg/kg SIN exhibited an increase in body temperature from 35.0 °C to 35.9 °C, 36.0 °C and 36.2 °C, respectively (Fig. 5A). Additionally, cromolyn, tranilast, and cetirizine significantly reduced histamine concentrations in the plasma of animals treated with 200 mg/kg SIN from 5.5 μg/ml to 3.1, 1.0 and 0.9 μg/ml, respectively (Fig. 5B). Significant amelioration of lung injury was observed in animals treated with these mast cell stabilizers, exhibiting reduced immune cell infiltration in the lung tissues (Fig. 5C). Given that IL-33 is a critical cytokine in the initiation and exacerbation of inflammatory responses and histamine release in mouse mast cells, we further examined whether the inhibitory effect of three mast cell stabilizers on histamine release resulted from reduction of IL-33 secretion. As shown in Fig. 5D and E, the levels of IL-33 in plasma and lung tissues were significantly increased in animals treated with SIN intravenously, whereas co-treatment with SIN and cromolyn, tranilast, or cetirizine induced reductions in IL-33 levels in plasma or lung tissues of rats. Collectively, mast cell stabilizers are effective in preventing SIN-triggered systemic HRARs.

Experimental model of IIR and animal groups [1]
Four sets of healthy male Kunming mice weighing 20–22 g were anesthetized by intraperitoneal injection of 10% chloral hydrate (3.0 ml/kg) after they were fasted for 16 h prior to surgery. Animals had free access to water prior to surgery. After ensuring an adequate depth of anesthesia, the mice were fixed in the supine position. In the IIR group (M group), the abdomen was opened and the superior mesenteric artery (SMA) was identified and clamped for 30 min. The clamp was then released and reperfusion of the splanchnic region was maintained for 3 days to observe survival rates or maintained for 3 h to define early small intestinal injury. In the sham-operated group (SH group), the abdomen was opened and the SMA was isolated but not clamped. In the other two treatment groups, mice subjected to IIR in the PreCr group and PostCr group were injected intravenously with Cromolyn sodium/CS (25 mg/kg in 0.1 ml) through the caudal vein at 15 min prior to ischemia and 15 min after releasing of the clamp, respectively. Mice in the SH and M groups received the same volumes of normal saline at 15 min prior to ischemia. In addition, pre-warmed normal saline (0.033 ml/g body weight) was administered subcutaneously to avoid fluid loss following surgery. The dose of CS/Cromolyn sodium was selected in accordance with previous publications.

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Induction and measurement of local HRARs in rat skins [2]
SIN induced local HRARs in rats was performed according to the methods described previously with modifications. SD rats were randomly divided into different groups. As positive control, rats were intradermally injected in the dorsal skin with anti-DNP-IgE (500 ng in 100 μl PBS). After 24 h, rats were challenged intravenously with or without 1 μg DNP-HSA containing 1% Evans blue dye. SIN (10 mg in 100 μl PBS) or PBS (100 μl) was intradermally injected in the dorsal skin of rats challenged with 1% Evans blue dye after 2 h. Cromolyn and cetirizine were dissolved in PBS. Tranilast was dissolved in CMC-Na (sodium carboxylmethyl cellulose). Cromolyn (30 mg/kg) was administered intravenously once before the challenge with DNP-HSA or injection of SIN or PBS. Cetirizine (15 mg/kg) and tranilast (400 mg/kg) were administered orally 1 h or 30 min before the challenge with DNP-HSA or injection of SIN or PBS. Vascular permeability was visualized 2 h later based on blue staining of the injection sites on the reverse side of the skin. Skin samples were harvested, and Evans blue dye was extracted from the tissues upon incubation at 55 °C for 48 h with 2 ml of formamide and quantified by OD at 610 nm.

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Induction and measurement of systemic HRARs in rats [2]
The experiment protocol was modified according to the previous description. Briefly, rats were intravenously injected with PBS or SIN at doses of 50 mg/kg, 100 mg/kg, and 200 mg/kg. Cromolyn, cetirizine and tranilast were prepared as described above. Cromolyn (30 mg/kg) was administered intravenously once before injection of SIN or PBS. Cetirizine (15 mg/kg) and tranilast (400 mg/kg) were administered orally 1 h or 30 min before the injection of SIN or PBS. Changes in body temperature were monitored though rectal temperature every 30 min until recovery of normal body temperature. Plasma was collected in each experiment at different time intervals for different purposes. Rats were sacrificed 2 h later, and their lung tissues were collected for histological analysis or stored at −80 °C until later use. IL-4, IL-18, IL-33, and LTB4 production levels in the plasma were determined by ELISA according to the manufacturer’s instructions.

Absorption, Distribution and Excretion
1%
Most of the absorbed drug is excreted unchanged via the liver and kidneys within a few days, with no apparent metabolic degradation. The unabsorbed portion (approximately 80%) is recovered in the feces. Peak plasma concentrations are reached within minutes after inhalation, with a plasma half-life of 1 to 1.5 hours. Sodium Cromoglycate
The amount of sodium cromoglycate absorbed into the bloodstream after inhalation of a 20 mg dose appears not to produce any systemic pharmacological effects. Sodium Cromoglycate
A small amount of absorbed sodium cromoglycate is excreted unchanged via the liver and kidneys…approximately 10% of the 20 mg dose may remain in the inhaler after patient use…approximately 8% of the dose is absorbed into the bloodstream (primarily through the lungs, but also through the gastrointestinal tract). Cromolyn Disodium/
The metabolism of cromolyn was studied in 12 asthmatic patients. Peak plasma concentrations were reached within 15 minutes of inhalation of a 20 mg dose, with an average of 9.2 ng/mL. Rapid pulmonary absorption; most of the inhaled dose is swallowed. For more complete data on absorption, distribution, and excretion of clomoline (10 cases), please visit the HSDB record page. Metabolites/Metabolites: No metabolites were detected in humans and nine mammals after oral and intravenous administration. /Cromoline disodium/ Biological half-life: 1.3 hours. The metabolism of clomoline was studied in 12 asthmatic patients. The mean plasma half-life was 81 minutes.

Effects During Pregnancy and Lactation
◉ Overview of Use During Lactation
While there is currently no published data on the use of sodium cromoglycate during lactation, the concentration of sodium cromoglycate in breast milk is likely very low, and poor absorption by the infant's gastrointestinal tract is expected. The expert panel considers the use of sodium cromoglycate during lactation to be acceptable.
◉ Effects on Breastfed Infants
No relevant published information was found as of the revision date.
◉ Effects on Lactation and Breast Milk
No relevant published information was found as of the revision date.

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Drug Interactions This article briefly discusses studies on the lack of ion pair formation between sodium cromoglycate (sodium cromoglycate) and alkylbenzodimethylammonium ions in the rat intestine. Sodium cromoglycate/
This article analyzes the hygroscopic and desorption isotherms of sodium cromoglycate (sodium cromoglycate) and lactose cromoglycate. At a water content as high as 15%, the tensile and shear properties of sodium cromoglycate remained unaffected, as water was adsorbed into the interior of the sodium cromoglycate, leaving very little water on the particle surface. This study investigated the mechanisms of action of the mast cell stabilizers sodium cromoglycate and FPL-52694 as protective agents against ethanol-induced gastric mucosal injury in an isolated gastric compartment model. Different concentrations (10-80 mg/ml) of the two drugs were applied to the gastric mucosa before exposure to 40% ethanol. Both drugs significantly reduced ethanol-induced injury in a dose-dependent manner. After oral administration (80 mg/kg), both drugs significantly reduced gastric injury induced by subsequent oral administration of anhydrous ethanol. Indomethacin pretreatment did not significantly affect the protective effect of FPL-52694, but it partially reversed the protective effect of sodium cromoglycate. Changes in gastric leukotriene C4 synthesis were not correlated with the protective effects of either drug. After oral administration of ethanol, the number of mast cells in both the mucosa and connective tissue was significantly reduced. In the FPL-52694 or sodium cromoglycate pretreatment groups, the number of mucosal mast cells was not significantly different from that in rats not treated with ethanol. Furthermore, although ethanol-induced hemorrhagic injury was reduced by more than 95%, the number of mast cells in connective tissue remained significantly lower than in the ethanol-treated control group. Therefore, these results suggest that stimulation of gastric prostaglandin synthesis is not a key factor in the mechanism of action of FPL-52694, and neither drug appears to alleviate injury through a mechanism affecting gastric leukotriene C4 synthesis. This study further suggests that the protective effect provided by sodium cromoglycate or FPL-52694 pretreatment may be unrelated to the effects of these drugs on the mast cell population in gastric connective tissue. /Sodium Cromoglycate/
This study investigated the effects of histamine on the absorption and clearance of inhaled sodium cromoglycate (sodium cromoglycate). The study included 7 patients with mild asthma and airway hyperresponsiveness and 8 healthy subjects who inhaled either a placebo or histamine, followed by sodium cromoglycate. In the asthma group, inhaled histamine resulted in a mean 24% decrease in forced expiratory volume in one second (FEV1), but had no effect on healthy subjects. Compared with inhaled placebo, histamine increased initial pulmonary absorption of sodium cromoglycate, but did not affect the total amount of drug absorbed in asthmatic patients or healthy subjects. These observations suggest that the pharmacokinetics of inhaled drugs may be significantly influenced by inflammatory mediators at the site of airway drug absorption. /Sodium cromoglycate/
For more complete data on interactions of sodium cromoglycate (9 types), please visit the HSDB record page.

[1]. Treatment of mice with cromolyn sodium after reperfusion, but not prior to ischemia, attenuates small intestinal ischemia-reperfusion injury. Mol Med Rep, 2013. 8(3): p. 928-34.

[2]. Sinomenine-induced histamine release-like anaphylactoid reactions are blocked by tranilast via inhibiting NF-κB signaling. Pharmacol Res. 2017 Aug 31. pii: S1043-6618(17)30796-X.

[3]. Ng, G. and A. Ohlsson, Cromolyn sodium for the prevention of chronic lung disease in preterm infants. Cochrane Database Syst Rev, 2012. 6: p. CD003059.

Cromoglycine is a solid. (NTP, 1992)
Cromoglycine is a dicarboxylic acid, a dichromone derivative of glycerol. It is a potent mast cell stabilizer. It has the effects of a calcium channel blocker and an anti-asthmatic drug. It is a dicarboxylic acid belonging to the chromone class of compounds. It is the conjugate acid of cromoglycate (1-).
It is a chromone complex that works by inhibiting the release of chemical mediators from sensitized mast cells. It is used to prevent allergic and exercise-induced asthma, but is ineffective for existing asthma attacks.
Sodium cromoglycate is a mast cell stabilizer. The physiological action of sodium cromoglycate is achieved by reducing histamine release.
Sodium cromoglycate is a synthetic mast cell stabilizer with anti-inflammatory activity. Sodium cromoglycate may interfere with antigen-mediated calcium ion influx into mast cells. This prevents mast cell degranulation, thereby stabilizing mast cells and inhibiting the release of inflammatory mediators such as histamine and leukotrienes, which are involved in type I hypersensitivity reactions. Sodium cromoglycate also prevents eosinophils from releasing inflammatory mediators. Sodium cromoglycate is a cromoglycate complex whose mechanism of action is by inhibiting the release of chemical mediators from sensitized mast cells. It is used to prevent allergic asthma and exercise-induced asthma, but is ineffective for existing asthma attacks. See also: Sodium cromoglycate (in salt form). Indications: For the treatment of patients with bronchial asthma. Also used to treat vernal keratoconjunctivitis, vernal conjunctivitis, and vernal keratitis. Mechanism of Action: Sodium cromoglycate inhibits mast cell degranulation, thereby preventing the release of histamine and slow-reacting anaphylactic substances (SRS-A, mediators of type I hypersensitivity reactions). Sodium cromoglycate may also reduce the release of inflammatory leukotrienes. Sodium cromoglycate may act by inhibiting calcium ion influx. An important role of sodium cromoglycate is believed to be the inhibition of the degranulation response of lung mast cells to various stimuli, including the interaction of cell-bound IgE with specific antigens. …In vitro studies have shown that sodium cromoglycate significantly reduces the release of histamine and other particulate contents, as well as the production of leukotrienes. However, its efficacy and potency are highly dependent on the source of mast cells. ...Focusing on the ability of sodium cromoglycate to reverse various functional changes in leukocytes in the blood of asthmatic patients after allergen stimulation, such as increased expression of membrane-bound receptors. ...Low concentrations (100 nM) of sodium cromoglycate can completely inhibit the activation of human neutrophils, eosinophils, or monocytes by chemokines. The mechanism of action of sodium cromoglycate remains relatively unclear. Current research focuses primarily on the ability of sodium cromoglycate to reduce antigen-induced intracellular Ca²⁺ accumulation in sensitized mast cells. One biochemically relevant factor in sodium cromoglycate's reduction of histamine release from mast cells is enhanced phosphorylation of the 78,000 Dalton protein. Unfortunately, these observations were obtained at higher concentrations of sodium cromoglycate (50 to 200 μM), and their relationship with treatment response remains undetermined. For more complete data on the mechanisms of action of sodium cromoglycate (6 in total), please visit the HSDB record page.

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Therapeutic Uses
Anti-asthma Drugs
A significant proportion of children with chronic refractory asthma (mild or severe) experience partial or complete protection after oral inhalation of sodium cromoglycate. Sodium cromoglycate
…There is evidence that patients with extrinsic asthma known to be allergic to a certain exogenous allergen are more likely to respond to sodium cromoglycate than patients with endogenous asthma known to be allergic to a certain exogenous allergen. However, it is currently impossible to predict which patients will have a satisfactory response to sodium cromoglycate. Inhaling sodium cromoglycate shortly before exercise can reduce bronchoconstriction that subsequently occurs in some asthma patients. This effect may be enhanced if the patient receives continuous treatment. /Sodium cromoglycate/
For more complete data on the therapeutic uses of sodium cromoglycate (of 20 types), please visit the HSDB record page.

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Drug Warnings
There have been no reports of anaphylactic shock, vasculitis, or other serious adverse reactions in humans. Urticaria and maculopapular rash are rare but resolve upon discontinuation of the drug. Two patients developed eosinophilic pneumonia after inhaling sodium cromoglycate. /Disodium/
This article describes a case of severe bronchoconstriction in a 42-year-old male patient after inhaling sodium cromoglycate (clomoline).
This article presents a study of the incidence of adverse reactions (dermatitis, myositis, gastroenteritis) in 375 asthmatic patients using 0.5% sodium cromoglycate. Results showed an incidence of 2% for adverse reactions. Reactions were non-life-threatening and completely reversible.
A 13-year-old asthmatic patient developed severe nasal congestion after 4 weeks of treatment with sodium cromoglycate; symptoms resolved within 24 hours of discontinuation. Reactions recurred when sodium cromoglycate was reintroduced 3 days and 3 weeks after the initial attack.
For more complete data on drug warnings for sodium cromoglycate (25 total), please visit the HSDB record page.

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Pharmacodynamics
Sodium cromoglycate (USAN) is a synthetic compound that inhibits antigen-induced bronchospasm and is therefore used to treat asthma and allergic rhinitis. Sodium cromoglycate is used as an ophthalmic solution to treat conjunctivitis and can also be taken orally to treat systemic mastocytosis and ulcerative colitis. Sodium cromoglycate is an organic sodium salt, the disodium salt of cromoglyic acid. It can be used as an anti-asthmatic drug and as a drug allergen. It contains cromoglycate ions (2-). Sodium cromoglycate is the sodium salt form of sodium cromoglycate, a mast cell stabilizer with anti-inflammatory activity. Sodium cromoglycate may interfere with the transport of antigen-stimulated calcium ions across the mast cell membrane, thereby inhibiting the release of histamine, leukotrienes, and other substances that cause hypersensitivity reactions from mast cells. Sodium cromoglycate also inhibits the chemotaxis of eosinophils. Sodium cromoglycate is a cromoglycate complex whose mechanism of action is by inhibiting the release of chemical mediators from sensitized mast cells. It is used to prevent allergic and exercise-induced asthma, but is ineffective for existing asthma attacks. See also: Sodium cromoglycate (containing the active ingredient). In summary, treatment of mice with CS during early reperfusion (rather than before ischemia) showed good therapeutic effects on ischemia-induced ischemia-reperfusion injury (IIRI). Appropriate mast cell (MC) activation can suppress inflammation by degrading endothelin-1 (ET-1); however, sustained MC activation may exacerbate inflammation by releasing trypsin, histamine and pro-inflammatory cytokines. [1] ZQFTN is a drug preparation derived from the medicinal plant Sinmenium acutum and is recognized in China as an effective drug for the treatment of rheumatoid arthritis (RA). However, histamine-releasing anaphylactic reactions (HRARs) often occur in some patients. Therefore, it is necessary to establish an effective clinical protocol to manage such HRARs. In this study, rat models of systemic anaphylactic reactions (HRARs) and local cutaneous anaphylactic reactions (HRARs) were established. Vascular permeability and mast cell number were quantitatively analyzed by Evans blue staining and histological methods. The levels of histamine, leukotriene B4 (LTB4), and interleukin-33 (IL-33) in plasma were detected by ultra-high performance liquid chromatography-solid phase extraction-mass spectrometry (UHPLC-SPE-MS), enzyme-linked immunosorbent assay (ELISA), and immunohistochemistry, respectively. The results showed that simvastatin (SIN) could significantly induce systemic and local allergic reactions in rats, manifested as a significant decrease in body temperature, increased skin vascular permeability, lung tissue damage, and mast cell infiltration and elevated IL-33 expression in skin and lung tissue. Mechanistic studies have shown that tranilast can prevent simvastatin-induced allergic reactions by inhibiting H1 receptor gene expression and NF-κB signaling pathway. Our results indicate that mast cell membrane stabilizers and H1 receptor blockers can effectively prevent SIN-induced HRARs, while sodium cromoglycate, cetirizine, and tranilast can be used for clinical treatment of ZQFTN-induced HRARs. [2] Background: Chronic lung disease (CLD) is common in premature infants and has a complex etiology, including inflammation. Sodium cromoglycate is a mast cell stabilizer that inhibits neutrophil activation and neutrophil chemotaxis, and therefore may play a role in the prevention of chronic lung disease (CLD).
Objective: To determine the effect of prophylactic use of sodium cromoglycate on the occurrence of CLD, mortality, or a combined outcome of death and CLD within 28 days of birth in preterm infants at risk of CLD.
Search Methods: Relevant studies were identified using the Cochrane Neonatal Assessment Group search strategy. The Cochrane Central Registry of Controlled Trials (CENTRAL, Cochrane Library, Vol. 3, 2009), MEDLINE, EMBASE, CINAHL (as of July 2009), personal files, and reference lists of identified trials were searched. This update was performed on April 12, 2012, using the same databases. Additionally, on the same day, abstracts from the annual meetings of the Chinese Academy of Pediatrics (2000–2012) were searched on the PAS2View™ website and the Web of Science website, starting with two previously identified trials.
Inclusion Criteria: Randomized or quasi-randomized controlled clinical trials involving preterm infants. Sodium cromoglycate must be initiated within two weeks of birth. The intervention must include administration of sodium cromoglycate using a nebulizer or metered-dose inhaler (with or without a spacer) and be compared to placebo or no intervention. Included studies must include at least one of the following outcome measures: overall mortality, 28-day incidence of chronic lung disease (CLD), CLD incidence at 36 weeks of gestation (PMA), or a composite outcome of 28-day mortality or CLD.
Data Collection and Analysis: Standard Cochrane Collaboration methods were used; see the Cochrane Manual of Interventions for details. For binary outcome measures, hazard ratios (RR) and risk differences (RD) and their 95% confidence intervals (CI) were reported; for continuous data, the weighted mean difference (WMD) was reported. Meta-analyses were performed using fixed-effects models. Heterogeneity was tested using the I² statistic.
Main Results: Two eligible studies were included, but the number of infants included was small. Prophylaxis with sodium cromoglycate did not have a statistically significant effect on the composite outcome of 28-day mortality or CLD; chronic lung disease (CLD) occurring at 28 days or 36 weeks of gestational age; or CLD occurring in surviving infants at 28 days or 36 weeks of gestational age. Prophylaxis with sodium cromoglycate did not show statistically significant differences in overall neonatal mortality, air leak incidence, necrotizing enterocolitis, intraventricular hemorrhage, sepsis, and days of mechanical ventilation. No side effects were observed. Further research does not appear necessary. Authors’ Conclusion: There is currently no evidence from randomized trials that sodium cromoglycate plays a role in the prevention of CLD. Sodium cromoglycate is not recommended for the prevention of CLD in preterm infants. [3]

C23H16O11

468.36654

468.069

16110-51-3

Cromolyn sodium;15826-37-6;Cromoglicic acid-d5;2140317-08-2

2882

Colorless crystals from ethanol + ether

1.623

752.3ºC at 760 mmHg

241-242ºC

263.9ºC

1.08E-23mmHg at 25°C

1.681

2.114

3

11

8

34

835

0

OC(COC1=CC=CC2=C1C(C=C(C(O)=O)O2)=O)COC3=CC=CC4=C3C(C=C(C(O)=O)O4)=O

IMZMKUWMOSJXDT-UHFFFAOYSA-N

InChI=1S/C23H16O11/c24-11(9-31-14-3-1-5-16-20(14)12(25)7-18(33-16)22(27)28)10-32-15-4-2-6-17-21(15)13(26)8-19(34-17)23(29)30/h1-8,11,24H,9-10H2,(H,27,28)(H,29,30)

5-[3-(2-carboxy-4-oxochromen-5-yl)oxy-2-hydroxypropoxy]-4-oxochromene-2-carboxylic acid

cromolyn; Cromoglicic acid; 16110-51-3; Cromoglycic acid; Cromoglicate; Acido cromoglicico; Acide cromoglicique; Acidum cromoglicicum;

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

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

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)