NB001
(Synonyms: 腺嘌呤,HTS 09836) 目录号 : GC36701
NB001 (HTS 09836) 是一种腺苷酸环化酶 1 (AC1)抑制剂，通过调节 AC1 活性对神经和非神经疼痛起作用。
Cas No.:686301-48-4
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
NB001 (HTS 09836) is an adenylcyclase 1 (AC1) inhibitor which has effect on neural and non-neural pain by modulating AC1 activity[1]. AC1[1]
[1]. Min Zhuo. Method for treating neuronal and non-neuronal pain. US8124599B2.
| Cas No. | 686301-48-4 | SDF | |
| 别名 | 腺嘌呤,HTS 09836 | ||
| Canonical SMILES | OCCCCCNCCN1C=NC2=C(N)N=CN=C12 | ||
| 分子式 | C12H20N6O | 分子量 | 264.33 |
| 溶解度 | DMSO : 50 mg/mL (189.16 mM; Need ultrasonic) | 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 | 3.7831 mL | 18.9157 mL | 37.8315 mL |
| 5 mM | 0.7566 mL | 3.7831 mL | 7.5663 mL |
| 10 mM | 0.3783 mL | 1.8916 mL | 3.7831 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。
Analgesic effects of NB001 on mouse models of arthralgia
Mol Brain 2015 Oct 9;8(1):60.PMID:26452469DOI:10.1186/s13041-015-0151-9.
Our previous studies have demonstrated the critical roles of calcium-stimulated adenylyl cyclase 1 (AC1) in the central nervous system in chronic pain. In the present study, we examined the analgesic effects of NB001, a selective inhibitor of AC1, on animal models of ankle joint arthritis and knee joint arthritis induced by complete Freund's adjuvant injection. NB001 treatment had no effect on joint edema, stiffness, and joint destruction. Furthermore, the treatment failed to attenuate the disease progression of arthritis. However, NB001 treatment (3 mg/kg) significantly weakened joint pain-related behavior in the mouse models of ankle joint arthritis and knee joint arthritis. Results indicated that NB001 exhibited an analgesic effect on the animal models of arthritis but was not caused by anti-inflammatory activities.
Analgesic effects of adenylyl cyclase inhibitor NB001 on bone cancer pain in a mouse model
Mol Pain 2016 Sep 9;12:1744806916652409.PMID:27612915DOI:10.1177/1744806916652409.
Background: Cancer pain, especially the one caused by metastasis in bones, is a severe type of pain. Pain becomes chronic unless its causes and consequences are resolved. With improvements in cancer detection and survival among patients, pain has been considered as a great challenge because traditional therapies are partially effective in terms of providing relief. Cancer pain mechanisms are more poorly understood than neuropathic and inflammatory pain states. Chronic inflammatory pain and neuropathic pain are influenced by NB001, an adenylyl cyclase 1 (AC1)-specific inhibitor with analgesic effects. In this study, the analgesic effects of NB001 on cancer pain were evaluated. Results: Pain was induced by injecting osteolytic murine sarcoma cell NCTC 2472 into the intramedullary cavity of the femur of mice. The mice injected with sarcoma cells for four weeks exhibited significant spontaneous pain behavior and mechanical allodynia. The continuous systemic application of NB001 (30 mg/kg, intraperitoneally, twice daily for three days) markedly decreased the number of spontaneous lifting but increased the mechanical paw withdrawal threshold. NB001 decreased the concentrations of cAMP and the levels of GluN2A, GluN2B, p-GluA1 (831), and p-GluA1 (845) in the anterior cingulate cortex, and inhibited the frequency of presynaptic neurotransmitter release in the anterior cingulate cortex of the mouse models. Conclusions: NB001 may serve as a novel analgesic to treat bone cancer pain. Its analgesic effect is at least partially due to the inhibition of AC1 in anterior cingulate cortex.
Human safety study of a selective neuronal adenylate cyclase 1 inhibitor NB001 which relieves the neuropathic pain and blocks ACC in adult mice
Mol Pain 2022 Apr;18:17448069221089596.PMID:35266830DOI:10.1177/17448069221089596.
Calcium-dependent, neuronal adenylyl cyclase subtype 1 (AC1) is critical for cortical potentiation and chronic pain. NB001 is a first-in-class drug acting as a selective inhibitor against AC1. The present study delineated the pharmacokinetic (PK) properties of human-used NB001 (hNB001) formulated as immediate-release tablet. This first-in-human (FIH) study was designed as randomized, double-blind, placebo-controlled trial. hNB001 showed placebo-like safety and good tolerability in healthy volunteers. A linear dose-exposure relationship was demonstrated at doses between 20 mg and 400 mg. The relatively small systemic exposure of hNB001 in human showed low bioavailability of this compound through oral administration, which can be improved through future dosage research. Food intake had minimal impact on the absorption of hNB001 tablet. Animal experiments further confirmed that hNB001 had strong analgesic effect in animal models of neuropathic pain. In brain slice prepared from the anterior cingulate cortex (ACC), bath application of hNB001 blocked the induction of long-term potentiation (LTP). These results from both rodents and human strongly suggest that hNB001 can be safely used for the future treatment of different types of chronic pain in human patients.
Isolation of nitrobenzene degrading strain Pseudomonas NB001 and application in the bioremediation of polluted water body
J Environ Sci Health A Tox Hazard Subst Environ Eng 2012;47(1):70-6.PMID:22217084DOI:10.1080/10934529.2012.629583.
A bacterium using nitrobenzene (NB) as a sole source of carbon, nitrogen and energy was isolated from NB-contaminated water body by the enrichment technology. It was identified as Pseudomonas NB001 by the phylogenetic analysis based on 16S rDNA sequence and the biochemical and physiological characteristics. Degradation of NB by strain NB001 was concomitant with the release of nitrite. Activities of catechol2,3-dioxygenase in strain NB001 cells grown in the culture fluid were higher than that in cells under any other conditions (P < 0.05). Under the pure culture conditions, 98.4% of NB at initial concentration of 50 mg L(-1) was removed in 136 hours. Glucose at starting concentration of 100 mg L(-1) delayed the onset of the exponential phase of NB degradation and weakened the degradation ability of per cell in the pure culture systems. In the river water, 89.5% of NB was degraded in 8 days. Suspended matter obviously increased the degradation rate of NB in the early stages, but decreased in the final stages. Cd(2+) and Hg(2+) significantly weakened the ability of the strain to degrade NB at initial concentrations of 10.0 mg L(-1) and 5.0 mg L(-1), respectively. The results would offer useful information for the application of strain NB001 in the bioremediation or the control of NB-contaminated environment.
Effects of NB001 and gabapentin on irritable bowel syndrome-induced behavioral anxiety and spontaneous pain
Mol Brain 2014 Jun 16;7:47.PMID:24935250DOI:10.1186/1756-6606-7-47.
Irritable bowel syndrome (IBS) is characterized by recurrent abdominal discomfort, spontaneous pain, colorectal hypersensitivity and bowel dysfunction. Patients with IBS also suffer from emotional anxiety and depression. However, few animal studies have investigated IBS-induced spontaneous pain and behavioral anxiety. In this study, we assessed spontaneous pain and anxiety behaviors in an adult mouse model of IBS induced by zymosan administration. By using Fos protein as a marker, we found that sensory and emotion related brain regions were activated at day 7 after the treatment with zymosan; these regions include the prefrontal cortex, anterior cingulate cortex, insular cortex and amygdala. Behaviorally, zymosan administration triggered spontaneous pain (decreased spontaneous activities in the open field test) and increased anxiety-like behaviors in three different tests (the open field, elevated plus maze and light/dark box tests). Intraperitoneal injection of NB001, an adenylyl cyclase 1 (AC1) inhibitor, reduced spontaneous pain but had no significant effect on behavioral anxiety. In contrast, gabapentin reduced both spontaneous pain and behavioral anxiety. These results indicate that NB001 and gabapentin may inhibit spontaneous pain and anxiety-like behaviors through different mechanisms.