CB-52
目录号 : GC41311
A stable analog of Δ9-THC and AEA
Cas No.:869376-90-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
CB-52 is a stable analog of δ9-tetrahydrocannabinol (THC) and anandamide (AEA). It exhibits high affinity for the central cannabinoid (CB1) and peripheral cannabinoid (CB2) receptors with Ki values of 210 and 30 nM, respectively. In vitro, CB-52 behaves primarily as a CB1 receptor partial agonist and a CB2 receptor neutral antagonist.
| Cas No. | 869376-90-9 | SDF | |
| Canonical SMILES | OC1=CC(OCCCCCCCCCCC(NC2CC2)=O)=C(CCCCCC)C=C1 | ||
| 分子式 | C26H43NO3 | 分子量 | 417.6 |
| 溶解度 | DMF: 30 mg/ml,DMSO: 30 mg/ml,Ethanol: 50 mg/ml,Ethanol: PBS (pH 7.2)(1:2): 0.3 mg//ml | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.3946 mL | 11.9732 mL | 23.9464 mL |
| 5 mM | 0.4789 mL | 2.3946 mL | 4.7893 mL |
| 10 mM | 0.2395 mL | 1.1973 mL | 2.3946 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
In vitro and in vivo pharmacology of synthetic olivetol- or resorcinol-derived cannabinoid receptor ligands
Br J Pharmacol 2006 Oct;149(4):431-40.PMID:16953186DOI:10.1038/sj.bjp.0706888.
Background and purpose: We have previously reported the development of CB-25 and CB-52, two ligands of CB1 and CB2 cannabinoid receptors. We assessed here their functional activity. Experimental approach: The effect of the two compounds on forskolin-induced cAMP formation in intact cells or GTP-gamma-S binding to cell membranes, and their action on nociception in vivo was determined. Key results: CB-25 enhanced forskolin-induced cAMP formation in N18TG2 cells (EC50 approximately 20 nM, max. stimulation = 48%), behaving as an inverse CB1 agonist, but it stimulated GTP-gamma-S binding to mouse brain membranes, behaving as a partial CB1 agonist (EC50 =100 nM, max. stimulation = 48%). At human CB1 receptors, CB-25 inhibited cAMP formation in hCB1-CHO cells (EC50 = 1600 nM, max. inhibition = 68% of CP-55,940 effect). CB-52 inhibited forskolin-induced cAMP formation by N18TG2 cells (IC50 = 450 nM, max. inhibition = 40%) and hCB1-CHO cells (EC50 = 2600 nM, max. inhibition = 62% of CP-55,940 effect), and stimulated GTP-gamma-S binding to mouse brain membranes (EC50 = 11 nM, max. stimulation approximately 16%). Both CB-25 and CB-52 showed no activity in all assays of CB2-coupled functional activity and antagonized CP55940-induced stimulation of GTP-gamma-S binding to hCB2-CHO cell membranes. In vivo, both compounds, administered i.p., produced dose-dependent nociception in the plantar test carried out in healthy rats, and antagonised the anti-nociceptive effect of i.p. WIN55,212-2. In the formalin test in mice, however, the compounds counteracted both phases of formalin-induced nociception. Conclusions and implications: CB-25 and CB-52 behave in vitro mostly as CB1 partial agonists and CB2 neutral antagonists, whereas their activity in vivo might depend on the tonic activity of cannabinoid receptors.
Immune cell counts and risks of respiratory infections among infants exposed pre- and postnatally to organochlorine compounds: a prospective study
Environ Health 2008 Dec 4;7:62.PMID:19055819DOI:10.1186/1476-069X-7-62.
Background: Early-life chemical exposure may influence immune system development, subsequently affecting child health. We investigated immunomodulatory potentials of polychlorinated biphenyls (PCBs) and p,p'-DDE in infants. Methods: Prenatal exposure to PCBs and p,p'-DDE was estimated from maternal serum concentrations during pregnancy. Postnatal exposure was calculated from concentrations of the compounds in mother's milk, total number of nursing days, and percentage of full nursing each week during the 3 month nursing period. Number and types of infections among infants were registered by the mothers (N = 190). White blood cell counts (N = 86) and lymphocyte subsets (N = 52) were analyzed in a subgroup of infants at 3 months of age. Results: Infants with the highest prenatal exposure to PCB congeners CB-28, CB-52 and CB-101 had an increased risk of respiratory infection during the study period. In contrast, the infection odds ratios (ORs) were highest among infants with the lowest prenatal mono-ortho PCB (CB-105, CB-118, CB-156, CB-167) and di-ortho PCB (CB-138, CB-153, CB-180) exposure, and postnatal mono- and di-ortho PCB, and p,p'-DDE exposure. Similar results were found for pre- and postnatal CB-153 exposure, a good marker for total PCB exposure. Altogether, a negative relationship was indicated between infections and total organochlorine compound exposure during the whole pre- and postnatal period. Prenatal exposure to CB-28, CB-52 and CB-101 was positively associated with numbers of lymphocytes and monocytes in infants 3 months after delivery. Prenatal exposure to p,p'-DDE was negatively associated with the percentage of eosinophils. No significant associations were found between PCB and p,p'-DDE exposure and numbers/percentages of lymphocyte subsets, after adjustment for potential confounders. Conclusion: This hypothesis generating study suggests that background exposure to PCBs and p,p'-DDE early in life modulate immune system development. Strong correlations between mono- and di-ortho PCBs, and p,p'-DDE exposures make it difficult to identify the most important contributor to the suggested immunomodulation, and to separate effects due to pre- and postnatal exposure. The suggested PCB and p,p'-DDE modulation of infection risks may have consequences for the health development during childhood, since respiratory infections early in life may be risk factors for asthma and middle ear infections.
Hepatic microsomal cytochrome P450 enzyme activity in relation to in vitro metabolism/inhibition of polychlorinated biphenyls and testosterone in Baltic grey seal (Halichoerus grypus)
Environ Toxicol Chem 2003 Mar;22(3):636-44.PMID:12627653doi
Among other factors, cytochrome P450 (CYP) enzyme activity determines polychlorinated biphenyl (PCB) bioaccumulation, biotransformation, and toxicity in exposed species. We measured the oxidative metabolism in vitro of 12 PCB congeners, representing structural groups based on the number and position of the chlorine atoms, by the hepatic microsomes of one Baltic grey seal (Halichoerus grypus). Microsomal metabolism was observed for several PCBs with vicinal H atoms exclusively in the ortho and meta positions and without any ortho-Cl substituents (CB-15 [4,4'-Cl2] and CB-77 [3,3',4,4'-Cl4]), vicinal meta and para-H atoms (CB-52 [2,2',5,5'-Cl4], and -101 [2,2',4,5,5'-Cl5]) or with both characteristics in combination with either only one ortho-Cl (CB-26 [2,3',5-Cl3], CB-31 [2,4',5-Cl3]) or two ortho-Cl substituents (CB-44 [2,2',3,5'-Cl4]). To allocate PCB biotransformation to specific CYPs, the inhibitive effect of compounds with known CYP-specific inhibition properties was assessed on in vitro PCB metabolism and on regio- and stereospecific testosterone hydroxylase activities. Metabolic inhibition was considered relevant at concentrations < or = 1.0 microM because these inhibitors became decreasingly selective at higher concentrations. At < 1.0 microM, ellipticine (CYPIAI/2 inhibitor) selectively inhibited CB-15, -26, -31, and -77 metabolism, with no significant inhibition of CB-44, -52, and -101 metabolism. Inhibition of CB-52 and -101 metabolism by chloramphenicol (CYP2B inhibitor) started at 1.0 microM and maximized at about 100% at 10 microM. Ketoconazole (CYP3A inhibitor) appeared to selectively inhibit CB-26, -31, and -44 metabolism relative to CB-15, -77, and -52 at concentrations < or = 1.0 microM. Major testosterone metabolites formed in vitro were 2beta-(CYP3A), 6beta- (CYP3A, CYPIA), and 16beta- (CYP2B) hydroxytestosterone and androstenedione (CYP2B, CYP2C11). The CYP forms indicated are associated with the specific metabolism of testosterone in laboratory animals. Inhibition of 2beta- and 6beta-hydroxytestosterone formation at ellipticine and ketoconazole concentrations < or = 1.0 microM suggested that both inhibitors were good substrates of CYP3A-like enzymes in grey seal. Chloramphenicol (model for CYP2B) is apparently not a good inhibitor of CYPI A and CYP3A activities in grey seal because the chemical did not inhibit any metabolic route of testosterone at concentrations from 0.1 to 10 microM. Our findings demonstrated that at least CYP1A- and CYP3A-like enzymes in the liver of grey seals are capable of metabolizing PCBs with ortho-meta and/or meta-para vicinal hydrogens. A CYP2B form might also be involved, but this could not be proven by the results of our experiments. Defining the profiles of CYP enzymes that are responsible for PCB biotransformation is necessary to fully understand the bioaccumulation, toxicokinetics, and risk of PCB exposure in seals and other free-ranging marine mammals.
Profiles of polychlorinated biphenyls (PCBs) in cement kilns co-processing solid waste
Chemosphere 2017 May;174:165-172.PMID:28161517DOI:10.1016/j.chemosphere.2017.01.115.
Co-incineration of sewage sludge in cement kilns can be used for its disposal. In the present study, samples were collected from three cement production runs where sewage sludge and other wastes (e.g. municipal solid waste, waste acid and wet sewage sludge) were co-processed. The samples were analyzed for polychlorinated biphenyls (PCBs). The dioxin-like (dl)-PCB concentrations in the stack gases from run 1, 2, and 3 were 344.6, 548.7, and 104.3 pg m-3, respectively. The toxic equivalency (TEQs) values for runs 1, 2, and 3 were 5.6, 8.9, and 0.7 pg TEQ Nm-3, respectively. Calculation of net emissions for the three runs indicated that the co-incineration of other waste in addition to sewage sludge in cement kilns would not increase emission of the dl-PCBs. PCB concentrations in samples from the suspension boiler and humidifier tower, kiln-end bag filter, and cyclone preheater were much higher than those in samples from the kiln head area, indicating that these stages will be important for controlling PCB formation. Chlorinated biphenyl (CB)-77, CB-105 and CB-118 were the major dl-PCB congeners, CB-52, CB-101 were the major indicator PCB congeners, and tetra-CB to hexa-CB were the major homologues for the total input or output materials.
Polychlorinated biphenyls and their hydroxylated metabolites in placenta from Madrid mothers
Environ Sci Pollut Res Int 2012 Jan;19(1):139-47.PMID:21698361DOI:10.1007/s11356-011-0545-x.
Introduction: Concentrations and congener profiles of polychlorinated biphenyls (PCBs) and their hydroxylated metabolites (OH-PCBs) in placenta samples from a Madrid population (Spain) are reported. Structure dependent retentions of OH-PCBs are known to occur in both humans and wildlife, making it of interest to assess placental transfer of both parent compounds and their metabolites to the developing foetus. Results: The ΣPCB concentrations found in placenta samples were in the range 943-4,331 pg/g fresh weight (f.w.), and their hydroxylated metabolites showed a 20-time lower concentration level (53-261 pg/g f.w.). The PCB profiles were surprisingly dominated by CB-52 and CB-101 accounting for more than 44% of the total PCB concentration. This is indicating a source of exposure that is not yet identified. The OH-PCB profiles were dominated by 4-OH-CB187 and 4-OH-CB146, representing >50% of the ΣOH-PCB concentration of the placenta samples. Statistical analysis of the data revealed strong correlations between the PCB congeners, among some OH-PCBs, and between OH-PCB metabolites with a meta- and para- substitution pattern. Both PCB and OH-PCB concentrations presented homogeneous distribution, what allowed the establishment of a partial least squares model that correlated the concentrations of OH-PCB with those of PCBs in placenta samples. In addition, causal correlations were observed between the concentrations of OH-PCBs and those of their corresponding PCB precursors.