MSAB
目录号 : GC61093
MSAB is a selective inhibitor of Wnt/β-catenin signaling that binds to β-catenin, promoting its degradation, and specifically downregulates Wnt/β-catenin target genes. MSAB shows potent anti-tumor effects.
Cas No.:173436-66-3
Sample solution is provided at 25 µL, 10mM.
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MSAB is a selective inhibitor of Wnt/β-catenin signaling that binds to β-catenin, promoting its degradation, and specifically downregulates Wnt/β-catenin target genes. MSAB shows potent anti-tumor effects.
MSAB impedes RAW264.7 cells and human PMBCs differentiating into OCs. MSAB decreases the expression of β‐catenin in RAW264.7 and ARP1 WT cells.[2]
MSAB (10-20 mg/kg; i.p. daily for 2 weeks) inhibits tumor growth of Wnt-dependent cancer cells in xenograft mice and MMTV-Wnt1 transgenic mice.[3]
[1] So-Young Hwang, et al. Cell Rep. 2016 Jun 28;16(1):28-36. [2] Zhang Y, et al. Clin Transl Med. 2022 Feb;12(2):e684.
| Cas No. | 173436-66-3 | SDF | |
| Canonical SMILES | O=C(C1=CC=CC(NS(=O)(C2=CC=C(C=C2)C)=O)=C1)OC | ||
| 分子式 | C15H15NO4S | 分子量 | 305.35 |
| 溶解度 | DMSO: 250 mg/mL (818.73 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 | 3.2749 mL | 16.3747 mL | 32.7493 mL |
| 5 mM | 0.655 mL | 3.2749 mL | 6.5499 mL |
| 10 mM | 0.3275 mL | 1.6375 mL | 3.2749 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。
MSAB activates capsule production at the transcription level in Staphylococcus aureus
Microbiology (Reading) 2016 Mar;162(3):575-589.PMID:26781313DOI:10.1099/mic.0.000243.
Staphylococcus aureus produces several virulence factors that allow it to cause a variety of infections. One of the major virulence factors is the capsule, which contributes to the survival of the pathogen within the host as a way to escape phagocytosis. The production of the capsular polysaccharide is encoded in a 16 gene operon, which is regulated in response to several environmental stimuli including nutrient availability. For instance, the capsule is produced in the late- and post-exponential growth phases, but not in the early- or mid-exponential growth phase. Several regulators are involved in capsule production, but the regulation of the cap operon is still poorly understood. In this study, we show that MSAB activates the cap operon by binding directly to a 10 bp repeat in the promoter region. We show that despite the fact that MSAB is expressed throughout four growth phases, it only activates capsule production in the late- and post-exponential growth phases. Furthermore, we find that MSAB does not bind to its target site in the early and mid-exponential growth phases. This correlates with decreased nutrient availability and capsule production. These data suggest either that MSAB binding ability changes in response to nutrients or that other cap operon regulators interfere with the binding of MSAB to its target site. This study increases our understanding of the regulation of capsule production and the mechanism of action of MSAB.
MSAB and CodY Interact To Regulate Staphylococcus aureus Capsule in a Nutrient-Dependent Manner
J Bacteriol 2018 Aug 10;200(17):e00294-18.PMID:29941424DOI:10.1128/JB.00294-18.
Staphylococcus aureus has a complex regulatory network for controlling the production of capsule polysaccharide. In S. aureus, capsule production is controlled by several regulators in response to various environmental stimuli. Previously, we described MSAB as a new regulator that specifically binds to the cap promoter in a growth phase- or nutrient-dependent manner. In addition to MSAB, several other regulators have also been shown to bind the same region. In this study, we examined the interactions between MSAB and other nutrient-sensing regulators (CodY and CcpE) with respect to binding to the cap promoter in a nutrient-dependent manner. We observed that msaABCR and ccpE interact in a complex fashion to regulate capsule production. However, we confirmed that ccpE does not bind cap directly. We also defined the regulatory relationship between msaABCR and CodY. When nutrients (branched-chain amino acids) are abundant, CodY binds to the promoter region of the cap operon and represses its transcription. However, when nutrient concentrations decrease, MSAB, rather than CodY, binds to the cap promoter. Binding of MSAB to the cap promoter activates transcription of the cap operon. We hypothesize that this same mechanism may be used by S. aureus to regulate other virulence factors.IMPORTANCE Findings from this study define the mechanism of regulation of capsule production in Staphylococcus aureus Specifically, we show that two key regulators, MSAB and CodY, coordinate their functions to control the expression of capsule in response to nutrients. S. aureus fine-tunes the production of capsule by coordinating the activity of several regulators and by sensing nutrient levels. This study demonstrates the importance of incorporating multiple inputs prior to the expression of costly virulence factors, such as capsule.
Combination of Weight-Bearing Training and Anti-MSTN Polyclonal Antibody Improve Bone Quality In Rats
Int J Sport Nutr Exerc Metab 2016 Dec;26(6):516-524.PMID:27098383DOI:10.1123/ijsnem.2015-0337.
Weight-bearing exercise is beneficial to bone health. Myostatin (MSTN) deficiency has a positive effect on bone formation. We wondered if a combination of weight-bearing training and polyclonal antibody for MSTN (MSAB) would augment bone formation to a greater degree than single treatment. In this study, rats were randomly assigned to four groups: Control, weight-bearing training (WT), MSAB, and WT+MSAB. The trained rats ran at 15 m/min bearing with 35% of their body weight, 40 min/day (2 min of running followed by 2 min of rest), 6 days/week, for 8 weeks. The rats with MSAB were injected once a week with MSAB for 8 weeks. MicroCT analysis showed that compared with the MSAB group, WT+MSAB significantly enhanced cortical bone mineral density (BMD) (p < .01), bone volume over total volume (BV/TV) (p < .01), trabecular thickness (p < .05), and reduced trabecular separation (Tb.Sp) (p < .01). Compared with the WT group, WT+MSAB significantly increased trabecular BMD (p < .05), BV/TV (p < .05), and decreased Tb.Sp (p < .05). Three-point bending test demonstrated that MSAB failed to improve bone biomechanical properties (p > .05), weight-bearing training significantly increased energy absorption (p < .05) and elastic modulus (p < .05). However, when they combined, biomechanical properties including maximum load (p < .05), stiffness (p < .05), elastic modulus (p < .01) and energy absorption (p < .01) were all significantly enhanced. In conclusion, the combination of weight-bearing training and MSAB have a greater positive effect on bone than treatment with either MSAB or weight-bearing training alone, suggesting that resistance training in combination with MSTN antagonists could be an effective approach for improving bone health and reducing osteoporosis risk.
Inhibiting myostatin signaling prevents femoral trabecular bone loss and microarchitecture deterioration in diet-induced obese rats
Exp Biol Med (Maywood) 2016 Feb;241(3):308-16.PMID:26438721DOI:10.1177/1535370215606814.
Besides resulting in a dramatic increase in skeletal muscle mass, myostatin (MSTN) deficiency has a positive effect on bone formation. However, the issue about whether blocking MSTN can inhibit obesity-induced bone loss has not been previously investigated. In the present study, we have evaluated the effects of MSTN blocking on bone quality in high-fat (HF), diet-induced obese rats using a prepared polyclonal antibody for MSTN (MSAB). Twenty-four rats were randomly assigned to the Control, HF and HF + MSAB groups. Rats in the HF + MSAB group were injected once a week with purified MSAB for eight weeks. The results showed that MSAB significantly reduced body and fat weight, and increased muscle mass and strength in the HF group. MicroCT analysis demonstrated that obesity-induced bone loss and architecture deterioration were significantly mitigated by MSAB treatment, as evidenced by increased bone mineral density, bone volume over total volume, trabecular number and thickness, and decreased trabecular separation and structure model index. However, neither HF diet nor MSAB treatment had an impact on femoral biomechanical properties including maximum load, stiffness, energy absorption and elastic modulus. Moreover, MSAB significantly increased adiponectin concentrations, and decreased TNF-α and IL-6 levels in diet-induced obese rats. Taken together, blocking MSTN by MSAB improves bone quality in diet-induced obese rats through a mechanotransduction pathway from skeletal muscle, and the accompanying changes occurring in the levels of circulating adipokines and pro-inflammatory cytokines may also be involved in this process. It indicates that the administration of MSTN antagonists may be a promising therapy for treating obesity and obesity-induced bone loss.
Recommendations for myasthenia gravis clinical trials
Muscle Nerve 2012 Jun;45(6):909-17.PMID:22581550DOI:10.1002/mus.23330.
The recommendations for clinical research standards published in 2000 by a task force of the Medical Scientific Advisory Board (MSAB) of the Myasthenia Gravis Foundation of America (MGFA) were largely successful in introducing greater uniformity in the recording and reporting of MG clinical trials. Recognizing that changes in clinical trial design and implementation may increase the likelihood that new therapies are developed for MG, the MGFA MSAB Task Force here presents updated recommendations for the design and implementation of clinical trials in MG, including (a) the use of a quantitative measure, such as the MG-Composite, that is weighted for clinical significance and incorporates patient reported outcomes; (b) consideration of nontrial strategies; and (c) development of biomarkers that support mechanistic studies of pharmacotherapies. The hope is that these updated task force recommendations will expedite the development and acceptance of more effective and less noxious therapies for MG.