3-CPs (3-Carbethoxypsoralen)
(Synonyms: 3-Carbethoxypsoralen; 3-Ethoxycarbonylpsoralen) 目录号 : GC33999
3-CPs (3-Carbethoxypsoralen) 是一种血清型荚膜多糖，可干扰抗体介导的细菌杀伤。
Cas No.:20073-24-9
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
Kinase experiment: | To measure the inhibitory effect of releaseing type 3-CPs on bacteria killing, an OPKA is performed with the addition of culture supernatant or mouse serum obtained at 24 h following i.p. injection with 103 CFU of the S. pneumoniae WU2 strain. In each well, 10 μL of diluted rabbit serum is mixed with 10 μL of strain WU2 (1,000 CFU) and 10 μL of culture supernatant or mouse serum for 30 min at room temperature before HL-60 cells and complement are added. The percent inhibition of bacterial killing is compared to that with the OPKA with the addition of ΔCPS WU2 culture supernatant or naive mouse serum containing no 3-CPs[2]. |
References: [1]. Silva EB, et al. Modulation of the UVB-induced lethality by furocoumarins in Staphylococcus aureus. J Photochem Photobiol B. 2014 Jan 5;130:260-3. doi: 10.1016/j.jphotobiol.2013.11.012. | |
3-CPs is a serotype capsular polysaccharide which can interfere with antibody-mediated bacterial killing.
3-CPs displays protective effect against UVB damage in all concentrations tested[1]. About 50% inhibition of bacterial killing is observed when 12 ng of purified type 3 CPS is added to the OPKA. The addition of 30 μL of mouse serum post-i.p. infection with WU2 (containing 0.4 to 0.7 μg/mL released type 3 CPS) shows 26% to 52% inhibition of bacterial killing, comparable to what is observed when an equivalent amount of purified CPS is added[2].
[1]. Silva EB, et al. Modulation of the UVB-induced lethality by furocoumarins in Staphylococcus aureus. J Photochem Photobiol B. 2014 Jan 5;130:260-3. doi: 10.1016/j.jphotobiol.2013.11.012. [2]. Choi EH, et al. Capsular Polysaccharide (CPS) Release by Serotype 3 Pneumococcal Strains Reduces the Protective Effect of Anti-Type 3 CPS Antibodies.
| Cas No. | 20073-24-9 | SDF | |
| 别名 | 3-Carbethoxypsoralen; 3-Ethoxycarbonylpsoralen | ||
| Canonical SMILES | O=C(C1=CC2=CC3=C(OC=C3)C=C2OC1=O)OCC | ||
| 分子式 | C14H10O5 | 分子量 | 258.23 |
| 溶解度 | Soluble in DMSO | 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 | 3.8725 mL | 19.3626 mL | 38.7252 mL |
| 5 mM | 0.7745 mL | 3.8725 mL | 7.745 mL |
| 10 mM | 0.3873 mL | 1.9363 mL | 3.8725 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。
Action spectra for 8-methoxypsoralen and 3-Carbethoxypsoralen in skin fibroblasts in vitro
Arch Dermatol Res 1982;272(3-4):245-50.PMID:7165332DOI:10.1007/BF00509052.
8-methoxypsoralen (8-MOP) and 3-Carbethoxypsoralen (3-CPs) are known photoreagents which have been employed in the treatment of psoriasis. Using skin fibroblasts grown in vitro we have determined the action spectra of both compounds in the long ultraviolet range. Narrow-band interference filters were applied to a Xenon lamp. Reduction in methyl-3H-thymidine (3H-TdR) uptake served as a parameter for photoinhibited cells. The results show a linear increate of 8-MOP-mediated photoinhibition with increasing wavelengths; 3-CPs showed comparatively weak inhibitory rates at the lower wavelength range (349-365 nm). Possibly this is due to the formation of 3-CPs photoproducts which are unreactive with DNA. Compared to 8-MOP, the monofunctional photoreagent 3-CPs is a weak photoinhibitor.
Oxidative DNA damage photo-induced by 3-Carbethoxypsoralen and other furocoumarins. Mechanisms of photo-oxidation and recognition by repair enzymes
J Mol Biol 1989 Sep 20;209(2):297-314.PMID:2479751DOI:10.1016/0022-2836(89)90278-7.
DNA photosensitization by several furocoumarins (including 3-Carbethoxypsoralen (3-CPs), 8-methoxypsoralen (8-MOP), 5-methoxypsoralen (5-MOP) and angelicin was investigated by using DNA sequencing methodology. 3-CPs induces photo-oxidation of guanine residues leading to alkali-labile sites in DNA (revealed by hot piperidine), whereas 8-MOP, 5-MOP and angelicin do not. There is a preferential photo-oxidation of G when located on the 5' side of GG doublets, likely to reflect a better accessibility of the G moiety in such a context. Mechanisms operating via both radicals (type I) and singlet oxygen (type II) are involved in the photo-oxidation of G residues by 3-CPs. Photo-oxidized G residues are produced independently of the formation of photoadducts, and scavengers of singlet oxygen or radicals do not inhibit photobinding of 3-CPs to DNA. This leads us to propose that covalent photoadducts arise from the intercalated excited sensitizer molecules, whereas G photo-oxidations are produced either by electron transfer reactions involving bound 3-CPs or by energy transfer to molecular oxygen, thereby producing singlet oxygen that subsequently reacts with guanine bases. Quantification of both types of DNA lesions indicated that in vitro photo-oxidized G residues are produced in DNA by 3-CPs plus ultraviolet light at least to the same extent as photoadducts, under our conditions. A calf thymus redoxyendonuclease, equivalent to the endonuclease III of Escherichia coli, specific for oxidative DNA damages, recognizes and cleaves DNA at sites of photo-oxidized G residues. The extent of the cleavage by this enzyme was close to that observed by hot piperidine and followed the amount of photo-oxidized G residues produced when the lifetime of excited oxygen species is modified. The redoxyendonuclease did not incise DNA treated with 8-MOP, 5-MOP or angelicin plus ultraviolet light. The exonuclease III and endonuclease IV of E. coli also involved in the repair of oxidative DNA damage, convert the replicative form I of 3-CPs-treated DNA to replicative form II. This suggests that the lesions recognized by these enzymes are apurinic-like lesions. In view of the low toxicity and mutagenicity of 3-CPs, DNA photo-oxidation products induced by the photodynamic effect of 3-CPs are likely to be efficiently taken care of by the DNA repair system(s). It is clear that 3-CPs photo-induces several classes of DNA damage, including oxidative damage.(ABSTRACT TRUNCATED AT 400 WORDS)
Photochemotherapy (PUVA) of psoriasis using 3-Carbethoxypsoralen, a non-carcinogenic compound in mice
Br J Dermatol 1979 Oct;101(4):379-89.PMID:389271DOI:10.1111/j.1365-2133.1979.tb00015.x.
The carcinogenic risk of photochemotherapy (PUVA) with bi-functional furocoumarins such as 8-methoxypsoralen (8-MOP) which form cross-links in cellular DNA has initiated a search for active but less hazardous psoralens. A new compound, 3-Carbethoxypsoralen (3-CPs), studied in the yeast Saccharomyces cerevisiae (eukaryote), has been shown to be very photoactive on DNA and to form only mono-additions to DNA. These lesions appear to be more easily repaired than the cross-links induced by 8-MOP. 3-CPs produces less nuclear genetic events such as nuclear mutations and mitotic crossovers, but more cytoplasmic 'petite' mutations (damage to mitochondrial DNA) than 8-MOP. In mice it was demonstrated that after local or intra-peritoneal administration, in contrast to 8-MOP, 3-CPs is non-toxic, non-erythematogenic, and non-carcinogenic. A study of ten psoriatic patients had shown that local applications of 3-CPs plus UV-A exhibit about the same therapeutic activity for the clearing of psoriatic lesions as local treatment with 8-MOP plus UV-A, but without any localized hyperpigmentation.
Mutagenic effects of 3-Carbethoxypsoralen and 8-methoxypsoralen plus 365-nm irradiation in mammalian cells
Mutat Res 1983 Dec;124(3-4):287-97.PMID:6656829DOI:10.1016/0165-1218(83)90200-8.
Cell survival, i.e. colony-forming ability, and the induction of 6-thioguanine-resistant (6-TGr) mutants were determined in Chinese hamster V79 cells by using two photoreactive furocoumarins of photochemotherapeutic interest: the bifunctional compound 8-methoxypsoralen (8-MOP) and the monofunctional compound 3-Carbethoxypsoralen (3-CPs). To quantify the mutation induction in V79 cells mutants deficient in the enzyme hypoxanthine-guanine phosphoribosyl transferase (HGPRT) were selected with the purine analogue 6-thioguanine (6-TG). The effects of the compounds alone at 50 microM in the absence of light and those of 365-nm radiation (UVA) at doses of up to 6 kJm-2 were negligible. When exposed to equimolar concentrations of the compounds together with UVA, V79 cells were about 8 times more sensitive to 8-MOP-plus-UVA than to 3-CPs-plus-UVA. Per unit dose of UVA, 8-MOP was about 7 times more effective than 3-CPs for the induction of 6-TGr mutants. The induction followed about one-hit kinetics for 3-CPs and about two-hit kinetics for 8-MOP. At 50% survival the frequency of 6-TGr mutants induced by 8-MOP plus UVA and 3-CPs plus UVA differed by a factor of about 3.5. These results show a marked concordance with those obtained in the yeast Saccharomyces cerevisiae: both compound exhibited lethal and mutagenic activities but the monofunctional compound 3-CPs was less lethal and mutagenic than the bifunctional compound 8-MOP.
Enzymatic recognition and biological effects of DNA damage induced by 3-Carbethoxypsoralen plus UVA
Mutat Res 1993 Jun;294(1):43-50.PMID:7683757DOI:10.1016/0921-8777(93)90056-m.
The specific recognition of DNA modifications by repair endonucleases was used to characterize damage induced by 3-Carbethoxypsoralen (3-CPs) plus UvA in M13mp8 replicative form I (RF-I) DNA. Under the conditions used, 3-CPs plus UVA generates DNA base modifications which are recognized by the UvrABC complex and the Fpg protein of E. coli. The rate of formation of UvrABC sensitive sites is 3-4-fold higher than that of Fpg sensitive sites. In addition a small number of sites of base loss (sensitive to Nfo protein) were observed. M13mp8 RF-I DNA treated with 3-CPs plus UVA was tested for transfection efficiency in E. coli mutants defective in either Fpg protein and/or UvrABC complex. The survival of 3-CPs plus UVA damaged M13mp8 RF-I DNA was significantly reduced when transfected into uvrA mutants compared to that in the wild-type strain. On the other hand, the survival of 3-CPs plus UVA damaged RF-I DNA was not altered in fpg-1 mutants. These results show that nucleotide excision repair mediated by the UvrABC complex is the major repair pathway involved in the elimination of lethal lesions induced in DNA by 3-CPs plus UVA. Our data suggest that in vitro exposure of M13mp8 RF-I DNA to 3-CPs plus UVA produces predominantly thymine photoaddition and to a lesser extent guanine photooxidation partially due to singlet oxygen generated during photoreaction. The photoaddition products are primarly responsible for the observed lethal effect.