NAT
目录号 : GC67797NAT 是一种初始的NAMPT激活剂。NAMPT 是 NAD 回收途径中的限速酶，使其成为研究许多与 NAD 耗竭相关的疾病 (如神经退行性疾病) 的有吸引力的靶点。
Cas No.:831243-31-3
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
NAT is an initial hit of NAMPT activator. NAMPT is the rate-limiting enzyme in the NAD salvage pathway, which makes it an attractive target for the research of many diseases associated with NAD exhaustion such as neurodegenerative diseases[1].
[1]. Wang L, et al. Optimization of NAMPT activators to achieve in vivo neuroprotective efficacy [published online ahead of print, 2022 Mar 16]. Eur J Med Chem. 2022;236:114260.
| Cas No. | 831243-31-3 | SDF | Download SDF |
| 分子式 | C18H21NO3 | 分子量 | 299.36 |
| 溶解度 | DMSO : ≥ 100 mg/mL (334.05 mM) | 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 | 3.3405 mL | 16.7023 mL | 33.4046 mL |
| 5 mM | 0.6681 mL | 3.3405 mL | 6.6809 mL |
| 10 mM | 0.334 mL | 1.6702 mL | 3.3405 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。
An evolutionary history of the CoA-binding protein NAT/Ivy
Protein Sci 2022 Dec;31(12):e4463.PMID:36192822DOI:10.1002/pro.4463.
NAT/Ivy is a diverse and ubiquitous CoA-binding evolutionary lineage that catalyzes acyltransferase reactions, primarily converting thioesters into amides. At the heart of the NAT/Ivy fold is a phosphate-binding loop that bears a striking resemblance to that of P-loop NTPases-both are extended, glycine-rich loops situated between a β-strand and an α-helix. NAT/Ivy, therefore, represents an intriguing intersection between thioester chemistry, a putative primitive energy currency, and an ancient mode of phospho-ligand binding. Current evidence suggests that NAT/Ivy emerged independently of other cofactor-utilizing enzymes, and that the observed structural similarity-particularly of the cofactor binding site-is the product of shared constraints instead of shared ancestry. The reliance of NAT/Ivy on a β-α-β motif for CoA-binding highlights the extent to which this simple structural motif may have been a fundamental evolutionary "nucleus" around which modern cofactor-binding domains condensed, as has been suggested for HUP domains, Rossmanns, and P-loop NTPases. Finally, by dissecting the patterns of conserved interactions between NAT/Ivy families and CoA, the coevolution of the enzyme and the cofactor was analyzed. As with the Rossmann, it appears that the pyrophosphate moiety at the center of the cofactor predates the enzyme, suggesting that NAT/Ivy emerged sometime after the metabolite dephospho-CoA.
Assay of NAT Activity
Methods Mol Biol 2023;2576:213-224.PMID:36152189DOI:10.1007/978-1-0716-2728-0_17.
In animal tissues, N-acyltransferase (NAT) catalyzes the first reaction in the biosynthetic pathway of bioactive N-acylethanolamines, in which an acyl chain is transferred from the sn-1 position of the donor phospholipid, such as phosphatidylcholine, to the amino group of phosphatidylethanolamine, resulting in the formation of N-acylphosphatidylethanolamine. NAT has long been known to be stimulated by Ca2+ and hence referred to as Ca2+-dependent NAT. Later, this enzyme was identified as cPLA2ε (also referred to as PLA2G4E). On the other hand, members of the phospholipase A/acyltransferase (PLAAT) family (also known as HRAS-like suppressor family) show Ca2+-independent NAT activity. In this chapter, we describe (1) partial purification of Ca2+-dependent NAT from rat brain, (2) purification of recombinant cPLA2ε and PLAAT-2, and (3) NAT assay using radiolabeled substrate.
Trans-Causalizing NAT-Modeled Bayesian Networks
IEEE Trans Cybern 2022 May;52(5):3553-3566.PMID:32763860DOI:10.1109/TCYB.2020.3009929.
Conditional independence encoded in Bayesian networks (BNs) avoids combinatorial explosion on the number of variables. However, BNs are still subject to exponential growth of space and inference time on the number of causes per effect variable in conditional probability tables. A number of space-efficient local models exist that allow efficient encoding of dependency between an effect and its causes, and can also be exploited for improved inference efficiency. We focus on the Nonimpeding Noisy-AND Tree (NIN-AND Tree or NAT) models because of multiple merits. We present a novel framework, trans-causalization of NAT-modeled BNs, by which causal independence embedded in NAT models is exploited for more efficient inference. We show that trans-causalization is exact and yields polynomial space complexity. We demonstrate significant efficiency gain on inference based on lazy propagation and sum-product networks.
Neoadjuvant therapy for pancreatic cancer
Updates Surg 2022 Feb;74(1):35-42.PMID:34628591DOI:10.1007/s13304-021-01186-1.
Multimodal treatment including surgery and chemotherapy is considered the gold standard treatment of pancreatic cancer by most guidelines. Neoadjuvant therapy (NAT) has been seen as a possible treatment option for resectable, borderline resectable and locally advanced PaC. The aim of this paper is to offer a state-of-the-art review on neoadjuvant treatments in the setting of pancreatic ductal adenocarcinoma. A systematic literature search was performed using PubMed, Cochrane, Web of Science and Embase databases, in order to identify relevant studies published up to and including July 2021 that reported and analyzed the role of neoadjuvant therapy in the setting of pancreatic carcinoma. Most authors are concordant on the strong role of neoadjuvant therapy in the setting of borderline resectable pancreatic cancers. Recent randomized trials demonstrated improvement of R0 rate and survival after NAT in this setting. Patients with locally advanced cancers may become resectable after NAT, with better results than those obtained with palliative therapies. Even in the setting of resectable cancers, NAT is being evaluated by ongoing randomized trials. Chemotherapy regimens in the setting of NAT and response to NAT are discussed. NAT has an important role in the multimodal treatment of patients with borderline resectable pancreatic cancer. It has a role in patients with locally advanced tumors as it can allow surgical resection in a relevant proportion of patients. For resectable pancreatic cancers, the role of NAT is under evaluation by several randomized trials.
Neoadjuvant Chemotherapy in Pancreatic Cancer: An Appraisal of the Current High-Level Evidence
Pharmacology 2021;106(3-4):143-153.PMID:32966993DOI:10.1159/000510343.
At the time of diagnosis, only about 20% of patients with pancreatic ductal adenocarcinoma (PDAC) have resectable disease. PDAC treatment necessitates a multidisciplinary approach, and adjuvant chemotherapy after upfront resection is an established means of preventing recurrence. Neoadjuvant chemotherapy (NAT), originally introduced to downstage tumor size, is nowadays more frequently used for selection of patients with favorable tumor biology and to control potential micrometastases. While NAT is routinely applied in locally advanced (LA) PDAC, there is increasing evidence demonstrating benefits of NAT in borderline resectable (BR) PDAC. The concept of NAT has recently been tested in resectable PDAC, but to date NAT has been restricted to clinical trials, as the data are limited and no clear benefits have yet been shown in this patient group. This review summarizes the current evidence for NAT in resectable, BR, and LA PDAC, with a focus on high-level evidence and randomized controlled trials.