Histamine H₁ receptor

Osthol is an O-methylated coumarin present in plants, including Angelica pubescens, Cnidium monnieri, and Angelica archangelica. In rabbit platelets that have been cleaned, osthol prevents platelet aggregation and ATP release that is brought on by ADP, arachidonic acid, PAF, collagen, ionophore A23187, and thrombin. Through the extracellular signal-regulated kinase 1/2 and bone morphogenetic protein-2/p38 pathways, osteospot mediates cell differentiation in human osteoblast cells and holds promise as a treatment for osteoporosis. By making HBsAg more glycosylated, osteoporosis also inhibits the hepatitis B virus's secretion in cell culture. [3]

Local bone formation was significantly stimulated by subcutaneous injection of osthole at a dose of 5 mg/kg per day into mouse skulls (histological analysis of skull tissue samples collected 2 weeks after the last injection and stained with H&E Orange G). Osthole significantly influenced bone formation, according to morphological analysis, and microtubule inhibition of TN-16 was just as successful as it was in the earlier investigation. However, when osthole was taken daily at a dose of 1 mg/kg, no such effect was observed. The bone loss of the castration stent can be considerably reversible with an 8-week intraperitoneal injection of osthole. Histological analysis of L4 samples stained with trinitrophenol poinsettia revealed that castrate stents treated with osthole had partially recovered their trabecular structure. Osthole treatment dramatically increased trabecular volume, thickness, and total BMD while decreasing trabecular separation, according to morphological analysis [2].

On the first study day, participants' peripheral blood samples are drawn between 7 and 9 a.m. and transferred into grouping tubes containing K₃EDTA. And then they make fresh PBMCs. A solution of 1% heat-inactivated human AB serum, 1% gentamicin, and 0.25% PHA is added to isolated cells that are seeded on 24-well plates at a density of 1×10⁶ per well using RPMI-1640. A 24-hour period is given to each well before active reagents are added, with pure medium serving as the substance's control. After three additional days, cells are harvested[1].

Mice: Four-week-old ICR Swiss mice receive subcutaneous injections over the calvarial surface twice a day for five days straight, either with or without Osthole treatment. The doses are 1 and 5 mg/kg per day, with three mice per group. As a positive control, microtubule inhibitor TN-16 (5 mg/kg per day, subcutaneous injection, twice daily for 2 days; 3 mice per group) is used. Three weeks after the start of treatment, all the mice are put to sleep, and the calvariae are removed, preserved for two days in 10% phosphate-buffered formalin, decalcified for two weeks in 10% EDTA, and then embedded in paraffin. Hematoxylin and eosine orange G are used to cut and stain histologic sections. Using the OsteoMeasure System for histomorphometry, the amount of new bone over the calvarial surface is measured. In order to quantify the mineral appositional rate (MAR) and bone-formation rate (BFR), mice undergo intraperitoneal injections of 20 mg/kg of double calcein at days 7 and 14, following which they are put to death 7 days later. Plastic sections of the labeling are inspected. The calvarial samples that have been dissected are embedded in methyl methacrylate after being fixed in 75% ethanol. A fluorescent microscope is used to examine unstained transverse sections that have a thickness of 3 µm. With the OsteoMeasure System, MAR and BFR are measured.
Rats: The rats are thirty six-month-old female Sprague-Dawley rats. The rats are randomly assigned by body weight into three groups for the surgery (n=10): group 1 is a sham surgery followed by PBS vehicle treatment (sham+VEH); group 2 is an ovariectomy followed by vehicle treatment (OVX+VEH); and group 3 is an ovariectomy followed by Osthole treatment (OVX+OST). The rats are given an intraperitoneal nembutal injection (30 mg/kg) to induce anesthesia. The eight-week course of treatment is administered beginning one month following surgery. For eight weeks, either vehicle or Osthole (100 mg/kg daily) is taken orally once daily. Dual-energy X-ray absorptiometry is used to measure the total bone mineral density (BMD, g/m²) of the rats prior to their euthanasia at the end of the experiments. Then, the left femoral shafts are utilized for biomechanical testing, and the fourth lumbar vertebrae (L4) are dissected for histomorphometric and micro-computed tomographic (µCT) analysis.

Absorption, Distribution and Excretion
ETHNOPHARMACOLOGICAL RELEVANCE: Libanotis buchtormensis is the source of an important traditional medicine from Shaanxi province of China used in the treatment of many illnesses. Libanotis buchtormensis supercritical extract (LBSE) has analgesic, sedative and anti-inflammatory qualities. Osthole is one of the major bioactive components of LBSE; it is known for its significant anti-tumor, analgesic, and anti-inflammatory properties, it also alleviates hyperglycemia. AIM OF THE STUDY: The purpose of the present study was to compare the pharmacokinetics and tissue distribution of osthole in Sprague-Dawley (SD) rats after oral administration of pure osthole and LBSE. The two preparations were administered at the same osthole dose (approximately 130 mg/kg). The results should provide some guidance for the clinical applications of Libanotis buchtormensis. MATERIALS AND METHODS: Comparative pharmacokinetics and tissue distribution of osthole in SD rats after oral administration of pure osthole and LBSE were analyzed using reversed-phase high-performance liquid chromatography (RP-HPLC). All pharmacokinetic data were analyzed using 3P97 software. Samples of blood and internal organs (heart, liver, spleen, lungs and kidney) were collected and pretreated according to the experimental schedule. After pretreatment, plasma and tissue samples were extracted using ether-ethyl acetate mixture (3:1, v/v). The concentration of osthole in the plasma and tissues were determined using the RP-HPLC method. RESULTS: The procedure described in this paper shows good precision and stability and is suitable for the osthole assays in biological samples. We found that the average plasma concentration-time profile of osthole after oral administration of osthole and LBSE showed a single peak. There were also clear differences between plasma concentrations of osthole after oral administration of pure osthole and LBSE. Non-osthole ingredients in LBSE showed some pharmacokinetic interactions with osthole and hence decreased its absorption levels (p<0.05). Our results show different tissue distribution of osthole in the single and composite administration regimens. CONCLUSIONS: This study compares the pharmacokinetic characteristics and tissue distribution of osthole in rats after oral administration of pure osthole and LBSE; the results might be useful in clinical application of this traditional Chinese herbal medicine.
ETHNOPHARMACOLOGICAL RELEVANCE: Bushen Yizhi prescription (BSYZ) is a traditional Chinese compound prescription, which is commonly used in China for treating ShenXu and hypophrenia based on traditional Chinese medicine and Alzheimer's Disease according to modern Chinese medicine. Cnidium monnieri (L.) Cusson fruits (CM) is treated as the main herb of BSYZ, and its main active ingredient Osthole (OST) is considered as one of the major active ingredients of BSYZ. Even though OST plays an important role in the BSYZ its bioavailability is poor. In order to investigate whether the bioavailability of OST was influenced by BSYZ and CM extract, the comparative evaluations on pharmacokinetics of OST after oral administration of pure OST at different doses, CM and BSYZ extract were studied. MATERIALS AND METHODS: 30 rats were randomly assigned to five groups and orally administered with pure OST at different doses (15, 75 and 150 mg/kg), CM (15 mg/kg OST) and BSYZ (15 mg/kg OST) extract. At different predetermined time points after administration, the concentrations of OST in rat plasma were determined by using the HPLC-UV method, and main pharmacokinetic parameters were investigated. RESULTS: The results showed that the pharmacokinetic parameters of OST were significantly different (p<0.05) among the groups. The AUC(0 to t), AUC(0 to infinity) and Cmax of OST were significantly increased after oral administration of BSYZ extract, followed by CM extract, in comparison to pure osthole at different doses. CONCLUSIONS: This present study indicated that the bioavailability of pure OST after oral administration was extremely low and it was dramatically enhanced because of the synergistic effect of the traditional Chinese Bushen Yizhi prescription.
A simple high-performance liquid chromatographic method was developed to study the pharmacokinetics of osthole in rat plasma. After addition of an internal standard (paeonol), plasma was deproteinized by acetonitrile for sample clean-up. The drugs were separated on a reversed-phase column and detected by UV absorption at 323 nm. Acetonitrile-water-diethylamine (50:50:0.1, v/v/v) (pH 3.0, adjusted with orthophosphoric acid) was used as the mobile phase. It was applied to the pharmacokinetic study of osthole in rats after a dose of 10 mg/kg by intravenous administration. A biphasic phenomenon with a rapid distribution followed by a slower elimination phase was observed from the plasma concentration-time curve.

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Metabolism / Metabolites
Osthole is an active ingredient and one of the major coumarin compounds that were identified in the genus Cnidium moonnieri (L.) Cussion, the fruit of which was used as traditional Chinese medicine to treat male impotence, ringworm infection and blood stasis conventionally. Recent studies revealed that osthole has diverse pharmacological effects, such as improving male sexual dysfunction, anti-diabetes, and anti-hypertentions. The inhibition of thrombosis and platelet aggregation and protection of central nerve were also observed. On the other hand, the metabolism of osthole has not yet been investigated thoroughly. Herein the biotransformation of osthole in rat was investigated after oral administration of osthole by using efficient and sensitive ultra-performance liquid chromatography-tandem quadrupole-time of flight mass spectrometry (UPLC-QTOF/MS). Eighteen osthole metabolites and the parent drug were detected and identified in rat urine. Fourteen metabolites of osthole were identified and characterized for the first time. Structures of metabolites of osthole were elucidated by comparing fragment pattern under MS/MS scan and change of molecular weight with those of osthole. The main phase I metabolic pathways were summed as 7-demethylation, 8-dehydrogenation, hydroxylation on coumarin and 3,4-epoxide. Sulfate conjugates were detected as phase II metabolites of osthole.
The biotransformation of osthole (1) by Alternaria longipes was carried out, and five transformed products were obtained in the present research work. Based on their extensive spectral data, the structures of these metabolites were characterized as 4'-hydroxyl-osthole (2), 4'-hydroxyl-2',3'-dihydroosthole (3), 2',3'-dihydroxylosthole (4), osthole-4'-oic acid methyl ester (5), and osthole-4'-oic acid glucuron-1-yl ester (6), respectively. Among them, products 5 and 6 were new compounds.

Toxicity Summary
IDENTIFICATION AND USE: Osthole is a natural product found in several medicinal plants such as Cnidium monnieri and Angelica pubescens. It has been tested as an experimental therapy. HUMAN STUDIES: Osthole has been reported to have antitumor activities via the induction of apoptosis and inhibition of cancer cell growth and metastasis. Studies in human colon cancer cell lines demonstrated that p53 was activated followed by generation of reactive oxygen species and activation of c-Jun N-terminal kinase. ANIMAL STUDIES: In vitro and in vivo experimental results have revealed that osthole demonstrates multiple pharmacological actions including neuroprotective, osteogenic, immunomodulatory, anticancer, hepatoprotective, cardiovascular protective, and antimicrobial activities. Osthole and other coumarins showed high activity in the inhibition of the mutagenicity of benzo[a]pyrene. ECOTOXICITY STUDIES: There was an increase in the morphological abnormalities in D. rerio embryo due to osthol over time. Coagulation, delayed hatching, yolk sac edema, pericardial edema, and pigmentation were observed in embryos at 24-48 hours. Symptoms of scoliosis and head edema occurred after 72 hours. In addition, bent tails, ocular defects, and symptoms of collapse were observed in fertilized embryo tissue within 96 hours. Ocular defects and pigmentation were the additional symptoms observed in this study.

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Interactions
Acetaminophen (APAP) overdose leads to severe hepatotoxicity. Osthole, a natural coumarin found in traditional Chinese medicinal herbs, has therapeutic potential in the treatment of various diseases. In this study, we investigated the effects of osthole against APAP-induced hepatotoxicity in mice. Mice were administered osthole (100 mg/kg per day, ip) for 3 d, then on the fourth day APAP (300 mg/kg, ip) was co-administered with osthole. The mice were euthanized post-APAP, their serum and livers were collected for analysis. Pretreatment with osthole significantly attenuated APAP-induced hepatocyte necrosis and the increases in ALT and AST activities. Compared with the mice treated with APAP alone, osthole pretreatment significantly reduced serum MDA levels and hepatic H2O2 levels, and improved liver GSH levels and the GSSG-to-GSH ratio. Meanwhile, osthole pretreatment markedly alleviated the APAP-induced up-regulation of inflammatory cytokines in the livers, and inhibited the expression of hepatic cytochrome P450 enzymes, but it increased the expression of hepatic UDP-glucuronosyltransferases (UGTs) and sulfotransferases (SULTs). Furthermore, osthole pretreatment reversed APAP-induced reduction of hepatic cAMP levels, but pretreatment with H89, a potent selective PKA inhibitor, failed to abolish the beneficial effect of osthole, whereas pretreatment with L-buthionine sulfoximine, a GSH synthesis inhibitor, abrogated the protective effects of osthole on APAP-induced liver injury, and abolished osthole-caused alterations in APAP-metabolizing enzymes. In cultured murine primary hepatocytes and Raw264.7 cells, however, osthole (40 umol/L) did not alleviate APAP-induced cell death, but it significantly suppressed APAP-caused elevation of inflammatory cytokines. Collectively, we have demonstrated that osthole exerts a preventive effect against APAP-induced hepatotoxicity by inhibiting the metabolic activation of APAP and enhancing its clearance through an antioxidation mechanism.
Inflammation and oxidative stress are implicated in the development of neurodegenerative diseases. Osthole is a compound that is extracted from She Chuang Zi, which is a type of traditional Chinese medicine. Osthole has previously been demonstrated to exhibit anticancer activities and has a low toxicity. However, to the best of our knowledge, the anti-inflammatory effects of osthole in microglial cells have not been investigated extensively. The aim of the present study was to investigate the potential protective effects of osthole against inflammation induced by lipopolysaccharide (LPS) in microglial cells. The present study employed LPS-stimulated BV2 mouse microglia to establish an inflammatory cell model and to investigate the anti-inflammatory effects of osthole. Cells were pretreated with osthole for 1 hr prior to LPS (10 ug/mL) stimulation. At 6 hr after the addition of LPS, alterations in the levels of inflammatory factors, including tumor necrosis factor (TNF)-a, interleukin (IL)-6 and IL-1beta, were determined by ELISA. Furthermore, at 24 hr after the addition of LPS, western blot analysis was performed to analyze the alterations in the protein expression of nuclear factor-kappaB (NF-kappaB) p65, phosphorylated-NF-kappaB p65, nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase (HO)-1. The results demonstrated that the secretion of the inflammatory cytokines TNF-a, IL-6 and IL-1beta by LPS-stimulated BV2 cells was significantly reduced by osthole treatment. Simultaneously, osthole treatment inhibited the LPS-induced activation of the NF-kappaB signaling pathway. In addition, osthole upregulated the expression of Nrf2 and HO-1 in a dose-dependent manner. Based on these results, osthole may exhibit anti-inflammatory effects via the NF-kappaB and Nrf2 pathways, indicating that osthole has the potential to be developed into an effective anti-inflammatory drug.
Pulmonary arterial hypertension (PAH) is an insidious and progressive disease that is triggered by various cardiopulmonary diseases. Inflammation has an important role in the progression of PAH. Osthole (Ost) is a coumarin that has clear anti-inflammatory properties. The present study aimed to investigate the effects of Ost on PAH, and to explore the mechanism underlying this effect. Using the monocrotaline (MCT)-induced PAH rat model, the effects of Ost on PAH were investigated. Rats were subcutaneously administered a single dose of MCT (50 mg/kg) to establish the PAH model, followed by daily treatment with Ost (10 or 20 mg/kg) by gavage for 28 days. The mean pulmonary arterial pressure (mPAP) was measured and histological analysis was performed. The results demonstrated that Ost significantly decreased mPAP, and reduced thickening of the pulmonary artery, compared with in rats in the MCT group. To further determine whether the effects of Ost on MCT-induced PAH were associated with inflammatory responses, the nuclear factor-kappaB (NF-kappaB) p65 signaling pathway was investigated by western blot analysis. The results demonstrated that Ost increased inhibition of the NF-kappaB p65 signaling pathway. In conclusion, the results of the present study demonstrate that Ost may suppress the progression of MCT-induced PAH in rats, which may be, at least partially, mediated through modulation of the NF-kappaB p65 signaling pathway.
Osthole, a natural coumarin found in traditional Chinese medicinal plants, has shown multiple biological activities. In the present study, we investigated the preventive effects of osthole on inflammatory bowel disease (IBD). Colitis was induced in mice by infusing TNBS into the colonic lumen. Before TNBS treatment, the mice received osthole (100 mg/kg par day, ip) for 3 d. Pretreatment with osthole significantly ameliorated the clinical scores, colon length shortening, colonic histopathological changes and the expression of inflammatory mediators in TNBS-induced colitis. Pretreatment with osthole elevated serum cAMP levels; but treatment with the PKA inhibitor H89 (10 mg/kg per d, ip) did not abolish the beneficial effects of osthole on TNBS-induced colitis. In mouse peritoneal macrophages, pretreatment with osthole (50 umol/L) significantly attenuated the LPS-induced elevation of cytokines at the mRNA level; inhibition of PKA completely reversed the inhibitory effects of osthole on IL-1beta, IL-6, COX2, and MCP-1 but not on TNFa. In Raw264.7 cells, the p38 inhibitor SB203580 markedly suppressed LPS-induced upregulation of the cytokines, whereas the PKA inhibitors H89 or KT5720 did not abolish the inhibitory effects of SB203580. Moreover, in LPS-stimulated mouse peritoneal macrophages, SB203580 strongly inhibited the restored expression of IL-1beta, IL-6, COX2, and MCP-1, which was achieved by abolishing the suppressive effects of osthole with the PKA inhibitors. Western blot analysis showed that osthole significantly suppressed the phosphorylation of p38, which was induced by TNBS in mice or by LPS in Raw264.7 cells. Inhibition of PKA partially reversed the suppressive effects of osthole on p38 phosphorylation in LPS-stimulated cells. Collectively, our results suggest that osthole is effective in the prevention of TNBS-induced colitis by reducing the expression of inflammatory mediators and attenuating p38 phosphorylation via both cAMP/PKA-dependent and independent pathways, among which the cAMP/PKA-independent pathway plays a major role.
For more Interactions (Complete) data for Osthole (9 total), please visit the HSDB record page.

[1]. Changes in gene expression induced by histamine, fexofenadine and osthole: Expression of histamine H1 receptor, COX-2, NF-κB, CCR1, chemokine CCL5/RANTES and interleukin-1β in PBMC allergic and non-allergic patients. Immunobiology . 2017 Mar;222(3):571-581.

[2]. Osthole stimulates osteoblast differentiation and bone formation by activation of beta-catenin-BMP signaling. J Bone Miner Res. 2010 Jun;25(6):1234-45.

[3]. Osthole pretreatment alleviates TNBS-induced colitis in mice via both cAMP/PKA-dependent and independent pathways. Acta Pharmacol Sin. 2017 Aug;38(8):1120-1128.

[4]. Osthole: A Review on Its Bioactivities, Pharmacological Properties, and Potential as Alternative Medicine. Evid Based Complement Alternat Med. 2015;2015:919616.

Osthole is a member of coumarins and a botanical anti-fungal agent. It has a role as a metabolite.
Osthole has been reported in Seseli hartvigii, Angelica japonica, and other organisms with data available.
See also: Angelica pubescens root (part of).

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Therapeutic Uses
/EXPL THER/ Osthole, an active coumarin extracted from the dried fruits of Cnidium monnieri (L.) Cusson, is known to possess a variety of pharmacological activities. In the present study, we investigated and illuminated the mechanisms underlying the protective effects of osthole in an experimental model of allergic asthma. Our results show that osthole treatment significantly reduced the OVA-induced increase in serum IgE and inflammatory cytokines (IL-4, IL-5, IL-13) in bronchoalveolar lavage fluid (BALF), and decreased the recruitment of inflammatory cells in BALF and the lung. It also effectively attenuated goblet cell hyperplasia and mucus overproduction in lung tissue. In addition, western blot analysis demonstrated that osthole blocked NF-kappaB activation, which may be associated with a reduction in inflammatory cytokine production. These data suggest that osthole attenuated OVA-induced allergic asthma inflammation by inhibiting NF-kappaB activation. The present study identified the molecular mechanisms of action of osthole, which support the potential pharmaceutical application of osthole treatment for asthma and other airway inflammation disorders.
/EXPL THER/ Hepatocellular carcinoma (HCC) accounts for approximately 90% of all cases of primary liver cancer, and the majority of patients with HCC are deprived of effective curative methods. Osthole is a Chinese herbal medicine which has been reported to possess various pharmacological functions, including hepatocellular protection. In the present study, we investigated the anticancer activity of osthole using HCC cell lines. We found that osthole inhibited HCC cell proliferation, induced cell cycle arrest, triggered DNA damage and suppressed migration in HCC cell lines. Furthermore, we demonstrated that osthole not only contributed to cell cycle G2/M phase arrest via downregulation of Cdc2 and cyclin B1 levels, but also induced DNA damage via an increase in ERCC1 expression. In addition, osthole inhibited the migration of HCC cell lines by significantly downregulating MMP-2 and MMP-9 levels. Finally, we demonstrated that osthole inhibited epithelial-mesenchymal transition (EMT) via increasing the expression of epithelial biomarkers E-cadherin and beta-catenin, and significantly decreasing mesenchymal N-cadherin and vimentin protein expression. These results suggest that osthole may have potential chemotherapeutic activity against HCC.
/EXPL THER/ Osthole (7-methoxy-8-isopentenoxy-coumarin), a compound extracted from Cnidiummonnieri (L.) Cusson seeds, has been found to exhibit potent therapeutic effects in cancer due to its ability to inhibit inflammation and cell proliferation. However, its effects on arterial wall hypertrophy-related diseases remain unclear. Therefore, in this study, we aimed to investigate the effects of Osthole on intimal hyperplasia in a rat model of carotid artery balloon injury. We established the balloon-induced carotid artery injury rat model in male Sprague-Dawley rats, after which we administered Osthole (20 mg/kg/day or 40 mg/kg/day) or volume-matched normal saline orally by gavage for 14 consecutive days. Intimal hyperplasia and the degree of vascular smooth muscle cell proliferation were then evaluated by histopathological examination of the changes in the carotid artery, as well as by examination of proliferating cell nuclear antigen (PCNA) expression. Tumor necrosis factor-alpha (TNF-a), interleukin-1beta (IL-1beta), transforming growth factor-beta (TGF-beta1) and PCNA mRNA expression levels were examined by real-time RT-PCR, while nuclear factor-kappaB (NF-kappaB (p65)), IkappaB-a, TGF-beta1 and phospho-Smad2 (p-Smad2) protein expression levels were analyzed by immunohistochemistry or western blot analysis. We found that Osthole significantly attenuated neointimal thickness and decreased the elevations in PCNA protein expression induced by balloon injury. Moreover, Osthole down-regulated the pro-inflammatory factors TNF-a and IL-1beta and NF-kappaB (p65), whose expression had been upregulated after balloon injury. Moreover, IkappaB-a protein expression levels increased following Osthole treatment. In addition, the elevations in TGF-beta1 and p-Smad2 protein expression induced by balloon injury were both significantly attenuated by Osthole administration. We concluded that Osthole significantly inhibited neointimal hyperplasia in balloon-induced rat carotid artery injury and that the mechanism by which this occurs may involve NF-kappaB, IL-1beta and TNF-alpha down-regulation, which alleviates the inflammatory response, and TGF-beta1/Smad2 signalling pathway inhibition.
/EXPL THER/ Multiple pharmacological applications of osthole have been previously recognized, including antioxidant, anti-inflammatory, anti-platelet and estrogenic effects, and resistance to pain. The present study investigated the protective effects of osthole against inflammation in a rat model of chronic kidney failure (CRF) and the underlying mechanisms. Osthole treatment with significantly reversed CRF-induced changes in serum creatinine, calcium, phosphorus and blood urea nitrogen levels in CRF rats. Male Sprague-Dawley rats (age, 8 weeks) received 200 mg/kg 2% adenine suspension to induce CRF in the model group. In the osthole-treated group, rats received 200 mg/kg 2% adenine suspension + osthole (40 mg/kg, intravenously). The results revealed that treatment with osthole significantly inhibited CRF-induced tumor necrosis factor-a, interleukin (IL)-8 and IL-6 expression, and suppressed nuclear factor-kappaB (NF-kappaB) protein expression in CRF rats. Osthole treatment significantly attenuated the protein expression of transforming growth factor-beta1 (TGF-beta1), reduced monocyte chemoattractant protein-1 activity and increased the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) ratio in CRF rats. These results suggested that osthole protects against inflammation in a rat model of CRF via suppression of NF-kappaB and TGF-beta1, and activation of PI3K/Akt/nuclear factor (erythroid-derived 2)-like 2 signaling. Therefore, osthole may represent a potential therapeutic agent for the treatment of CRF.
For more Therapeutic Uses (Complete) data for Osthole (18 total), please visit the HSDB record page.

C15H16O3

244.29

244.109

C, 73.75; H, 6.60; O, 19.65

484-12-8

Osthole-d3

10228

White to off-white solid powder

1.1±0.1 g/cm3

396.7±42.0 °C at 760 mmHg

83-84°C

167.6±22.5 °C

0.0±0.9 mmHg at 25°C

1.557

3.87

0

3

3

18

366

0

O1C(C([H])=C([H])C2C([H])=C([H])C(=C(C1=2)C([H])([H])/C(/[H])=C(\C([H])([H])[H])/C([H])([H])[H])OC([H])([H])[H])=O

MBRLOUHOWLUMFF-UHFFFAOYSA-N

InChI=1S/C15H16O3/c1-10(2)4-7-12-13(17-3)8-5-11-6-9-14(16)18-15(11)12/h4-6,8-9H,7H2,1-3H3

7-methoxy-8-(3-methylbut-2-enyl)chromen-2-one

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)

Solubility in Formulation 1: ≥ 2.5 mg/mL (10.23 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (10.23 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
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.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (10.23 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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