(-)-Denudatin B
(Synonyms: (-)-白玉兰亭B,Denudatin B) 目录号 : GC63940
(-)-Denudatin B 具有抗血小板作用，通过电压门控和受体调控的Ca2+通道抑制Ca2+内流，从而放松血管平滑肌。(-)-Denudatin B 通过抑制胶原蛋白和凝血酶诱导的磷酸肌苷分解，在高浓度下具有非特异性的抗血小板作用。
Cas No.:87402-88-8
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >97.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
(-)-Denudatin B is an antiplatelet agent. (-)-Denudatin B relaxed vascular smooth muscle by inhibiting the Ca2+ influx through voltage-gated and receptor-operated Ca2+ channels[1]. And (-)-Denudatin B has nonspecific antiplatelet action
[1]. Yu SM,et al. Vasorelaxing effect in rat thoracic aorta caused by denudatin B, isolated from the Chinese herb, magnolia fargesii. Eur J Pharmacol. 1990;187(1):39-47.
[2]. Teng CM, et al. Inhibition of thrombin- and collagen-induced phosphoinositides breakdown in rabbit platelets by a PAF antagonist--denudatin B, an isomer of kadsurenone. Thromb Res. 1990;59(1):121-130.
| Cas No. | 87402-88-8 | SDF | Download SDF |
| 别名 | (-)-白玉兰亭B,Denudatin B | ||
| 分子式 | C21H24O5 | 分子量 | 356.41 |
| 溶解度 | 储存条件 | 4°C, away from moisture and light | |
| 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 | 2.8058 mL | 14.0288 mL | 28.0576 mL |
| 5 mM | 0.5612 mL | 2.8058 mL | 5.6115 mL |
| 10 mM | 0.2806 mL | 1.4029 mL | 2.8058 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。
[Neolignans and lignan from Piper wallichii]
Zhongguo Zhong Yao Za Zhi 2010 Jan;35(2):180-2.PMID:20394289DOI:10.4268/cjcmm20100213.
To investigate the chemical constituents of the aerial part of Piper wallichii. Nine compounds were isolated by various chromatographic techniques and the structures were elucidated by their physicochemical properties and the spectral data analysis. Nine compounds were identified as one lignan (-)-galbelgin (1) and eight neolignans: denudatin B (2), hancinone D (3), (+)-licarin A (4), kadsurenone (5), wallichinine (6), hancinone C (7), hancinone B (8), (+)-burchellin (9). Compounds 1, 3, 4, 8, 9 were isolated from this plant for the first time.
[PAF antagonistic benzofuran neolignans from Piper kadsura]
Yao Xue Xue Bao 1993;28(5):370-3.PMID:8237383doi
In a continuing search for PAF antagonists, five benzofuran neolignans have been isolated from the aerial part of Piper kadsura (Choisy) Ohwi, a Chinese traditional drug used for the treatment of inflammation and rheumatic conditions. The structure determination was based upon spectroscopic analysis. Two of the neolignans were found to have new structures and were named as (-)-Denudatin B (the enantiomer of denudatin B, II) and kadsurenin M (7S,8S-3,4,3'-trimethoxy-7'-oxo-nor-8',9'-7.O. 4',8,5'-neolignan, V). The known compounds kadsurenon (I), (-)-acuminatin(III) and (+)-licarin A(IV) were also obtained from the same source. (-)-Denudatin B (II) showed potent PAF antagonistic activity in 3H-PAF receptor binding assay.
Species difference in the specific receptors of platelet activating factor
Biochem Pharmacol 1986 Dec 15;35(24):4511-8.PMID:3024653DOI:10.1016/0006-2952(86)90772-0.
Relative potencies of platelet activating factor (PAF) and PAF analogs and several PAF receptor antagonists when inhibiting the [3H]PAF specific binding to human and rabbit platelet membranes and membrane fragments of human lung tissues were compared. In rabbit platelets, L-652,731 was found to be most potent in the list of PAF receptor antagonists with an equilibrium inhibition constant (Ki) of 9.83 (+/- 2.92) X 10(-9) M followed by L-653,150 greater than kadsurenone congruent to Ono-6240 greater than ginkgolide B greater than CV-3988 greater than L-651,142, whereas in human platelets the relative potencies of these PAF receptor antagonists were as follows: Ono-6240 greater than L-653,150 congruent to L-652,731 congruent to kadsurenone greater than ginkgolide B greater than CV-3988 greater than L-651,142. Ono-6240 was the most potent one with a Ki of 4.86 (+/- 1.44) X 10(-8) M which was roughly two times more potent than that in rabbit platelets, whereas the affinity of L-652,731 was about ten times less in human platelets (Ki = 1.03 (+/- 0.15) X 10(-7) M) compared to that in rabbit platelets (Ki = 9.83 (+/- 2.92) X 10(-9) M). These variations between species among PAF antagonists strongly suggest that there exists a species difference at or near the binding site of the receptor of platelet activating factor. The relative potency of these PAF receptor antagonists in human lung membranes differed very little from that in human platelets and was found to be Ono-6240 greater than L-653,150 congruent to kadsurenone congruent to L-652,731 greater than ginkgolide B greater than CV-3988 greater than L-651,142. Even though C16-PAF showed slightly higher potency in human lung, and CV-3988 and Ono-6240 showed slightly lower, the difference was too small to suggest that there is a difference in the PAF receptors between human platelets and human lung tissues.
Stimulation of tumour necrosis factor release by cytotoxic analogues of platelet-activating factor
Immunology 1992 May;76(1):24-9.PMID:1628897doi
The capacity of cytotoxic analogues of platelet-activating factor (PAF) to stimulate tumour necrosis factor-alpha (TNF-alpha) synthesis and release by human monocytes was determined. Cell-associated TNF-alpha was quantified by protein immunoblotting and released TNF-alpha was quantified by cytotoxicity bioassay. Picomolar concentrations of methoxyPAF, SDZ 62-759, SDZ 68-826, SDZ 62-434 and SRI 62-834 induced a two- to fivefold increase in cell-associated and released TNF-alpha. These compounds were as potent as PAF for stimulating monocytes. In contrast, they lacked direct platelet-activating activity and inhibited platelet aggregation induced by PAF selectivity. The analogues inhibited PAF binding to platelets but not to monocytes. The PAF binding antagonists kadsurenone, BN52021 and WEB2086 inhibited TNF-alpha release induced by 10(-11) M PAF or methoxyPAF by a maximum of only 30-60% whereas they inhibited platelet aggregation by 10(-8) M PAF completely. Monocyte receptors for methoxyPAF were evaluated. Scatchard analysis of [3H]methoxyPAF binding to monocytes revealed large numbers of relatively low affinity receptors (Kd = 5.9 +/- 0.5 x 10(-7) M; 9.1 +/- 4.2 x 10(7) sites/monocyte). These values do not correspond to binding constants of monocyte receptors for PAF and do not account for monocyte activation by picomolar concentrations of methoxyPAF. Cytotoxic analogues of PAF stimulate TNF-alpha synthesis and release but they do not stimulate monocytes by interacting with PAF receptors.