TDN345
目录号 : GC31038
TDN345A是一种Ca2+拮抗剂，主要用于治疗血管和老年痴呆疾病，例如阿尔茨海默症。
Cas No.:134069-68-4
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
Animal experiment: | Male Mongolian gerbils (50-70 g body weight) are anesthetized lightly by ether inhalation. A 1-2 cm midline throat incision provided access to both carotid arteries, which are clamped with microaneurysm clamps immediately after recovery from anesthesia. Sixty minutes before occlusion, TDN-345 (0.3 or 1.0 mg/kg suspended in a 5% gum arabic solution or 0.1 or 0.3 mg/kg with 1% NaHCO3 suspended in a 5% gum arabic solution) or vehicle is administered orally. After 15 min of bilateral carotid artery occlusion, the clamps are removed. Ninety minutes after reperfusion, TDN-345 or vehicle is again administered orally. The body temperature is maintained at 37°C during the experimental period using a heating pad. The experiments are performed in nine to 15 animals in each group. Animal survival is observed 8 h and 7 days after reperfusion, and neurological signs are evaluated according to the scoring system as an ischemic neurological score for 5 h after the ischemic insult from an area under the time-neurological deficit score curve (AUCreperfusion (0-300 min)) (hair roughed up or tremor, obtunded, paucity of move, 1; ptosis, seizure, 2; head cocked, eyes fixed open, splayed out hind limbs, extreme rotation, circling behavior, rolling seizure, 3; coma, 6; death, 34). Nine to 15 animals are used in each experimental group. |
References: [1]. Fukumoto H, et al. The novel compound TDN-345 induces synthesis/secretion of nerve growth factor in C6-10A glioma cells. Brain Res. 1997 Nov 7;774(1-2):87-93. | |
TDN345 is a Ca2+ antagonist, used for the treatment of vascular and senile dementia including Alzheimer's disease.
TDN-345 (10 μM) significantly increases the intracellular NGF content in the time-course study. TDN-345 induces NGF synthesis/secretion at the concentrations of 0.1 μM; statistically significant at 1 μM. The ED50 is 0.88 μM[1].
TDN-345 (0.1-1.0 mg/kg, p.o.) dose-dependently decreases the mortality and ischemic neurological deficit score when administered orally twice, 60 min before ischemia and 90 min after recirculation. Additionally, TDN-345 (0.2 or 1.0 mg/kg, p.o. once daily for 3 weeks after the onset of stroke) decreases the mortality and recurrence of stroke in SHRSP[2].
[1]. Fukumoto H, et al. The novel compound TDN-345 induces synthesis/secretion of nerve growth factor in C6-10A glioma cells. Brain Res. 1997 Nov 7;774(1-2):87-93. [2]. Nakayama T, et al. Beneficial effects of TDN-345, a novel Ca2+ antagonist, on ischemic brain injury and cerebral glucose metabolism in experimental animal models with cerebrovascular lesions. Brain Res. 1997 Jul 11;762(1-2):203-10.
| Cas No. | 134069-68-4 | SDF | |
| Canonical SMILES | O=C(N1C(C)(C)C)OC2(CCN(CCCC(C3=CC=C(F)C=C3)C4=CC=C(F)C=C4)CC2)C1=C | ||
| 分子式 | C28H34F2N2O2 | 分子量 | 468.58 |
| 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 | 2.1341 mL | 10.6705 mL | 21.3411 mL |
| 5 mM | 0.4268 mL | 2.1341 mL | 4.2682 mL |
| 10 mM | 0.2134 mL | 1.0671 mL | 2.1341 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。
The novel compound TDN-345 induces synthesis/secretion of nerve growth factor in C6-10A glioma cells
A novel compound, TDN-345, not bearing catechol moiety, induced NGF synthesis/secretion in C6-10A glioma cells. Both intracellular and extracellular nerve growth factor (NGF) protein levels increased within 3 h and reached a maximum around 12 h after the addition of TDN-345. The induction of NGF synthesis/secretion by TDN-345 occurred in a concentration-dependent manner, beginning with about 0.1 microM and reaching a maximum at 10 microM. The ED50 was 0.88 microM. The induction was accompanied by an increase in NGF mRNA but not beta-actin mRNA. In a time-course study, the NGF mRNA level was found to reach a maximum 2-3 h after the addition of TDN-345 and then to return to control levels. The induction occurred dose-dependently. The catecholaminergic compound epinephrine, which induces NGF synthesis/secretion, increased the intracellular cyclic AMP content by more than 1000-times at 10 microM. In contrast, TDN-345 did not cause such a prominent increase in cAMP even at 100 microM. These results indicate that TDN-345 induces NGF synthesis/secretion by increasing NGF mRNA expression, and the action of TDN-345 clearly differs from that of epinephrine, as it does not seem to involve cAMP as a second messenger. The results of the present study suggest the existence of a signal transduction pathway for NGF synthesis/secretion which is not mediated by cAMP.
Beneficial effects of TDN-345, a novel Ca2+ antagonist, on ischemic brain injury and cerebral glucose metabolism in experimental animal models with cerebrovascular lesions
The effects of TDN-345 on mortality and ischemic neurological deficit following transient global cerebral ischemia in Mongolian gerbils and also the rate of local cerebral glucose utilization (LCGU) in stroke-prone spontaneously hypertensive rats (SHRSP) with cerebrovascular lesions were investigated. In Mongolian gerbils, ischemia was produced by clamping the bilateral common carotid arteries for 15 min. TDN-345 (0.1-1.0 mg/kg) dose-dependently decreased the mortality and ischemic neurological deficit score when administered orally twice, 60 min before ischemia and 90 min after recirculation. Additionally, TDN-345 (0.2 or 1.0 mg/kg, p.o. once daily for 3 weeks after the onset of stroke) decreased the mortality and recurrence of stroke in SHRSP. To determine the site of action of TDN-345 in the brain, the rate of LCGU in various brain regions in SHRSP with stroke was examined using a [14C]2-deoxy-D-glucose method. The rate of LCGU decreased significantly in all the brain regions in SHRSP with stroke compared with Wistar-Kyoto (WKY) control rats, whereas the reduction in the rate of LCGU in SHRSP with stroke was prevented by TDN-345 treatment, especially in the sensorimotor cortex and locus coeruleus. These results suggest that TDN-345 has therapeutic efficacy in the treatment of cerebrovascular disease.