TMI 1
(Synonyms: WAY-171318) 目录号 : GC46026
An ADAM and MMP inhibitor
Cas No.:287403-39-8
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
TMI 1 is an inhibitor of disintegrin and metalloproteinase domain-containing protein 17 (ADAM17/TACE; IC50 = 8.4 nM in a cell-free enzyme assay).1 It inhibits matrix metalloproteinase-1 (MMP-1), -2, -7, -9, -13, and -14, as well as ADAM-TS-4 in vitro (IC50s = 6.6, 4.7, 26, 12, 3, 26, and 100 nM, respectively). It also inhibits ADAM8, -10, -12, and -17/TACE in cell-free enzyme assays with Ki values of 21, 16, 1.8, and 0.079 nM, respectively, with slow-binding inhibition of ADAM17/TACE but not the other ADAM enzymes.2 TMI 1 inhibits LPS-induced TNF-α secretion in Raw and THP-1 cells (IC50s = 40 and 200 nM, respectively), as well as in isolated human monocytes and whole blood (IC50s = 190 and 300 nM, respectively).1 It inhibits the production of TNF-α ex vivo in synovium isolated from the inflamed joints of patients with rheumatoid arthritis with IC50 values of less than 100 nM without inhibiting TNF-α expression in vitro. TMI 1 inhibits LPS-induced TNF-α production in mice (ED50 = 5 mg/kg) and reduces disease severity in mouse models of collagen-induced arthritis. It also decreases cell viability of (ED50s = 1.3-8.1 μM), and induces caspase-3/7 activity in, a variety of cancer cell lines and induces tumor apoptosis and reduces tumor growth in an MMTV-ErbB2/neu mouse model of breast cancer when administered at a dose of 100 mg/kg.3
|1. Zhang, Y., Xu, J., Levin, J., et al. Identification and characterization of 4-[[4-(2-butynyloxy)phenyl]sulfonyl]-N-hydroxy-2,2-dimethyl-(3S)thiomorpholinecarboxamide (TMI-1), a novel dual tumor necrosis factor-α-converting enzyme/matrix metalloprotease inhibitor for the treatment of rheumatoid arthritis. J. Pharmacol. Exp. Ther. 309(1), 348-355 (2004).|2. Moss, M.L., and Rasmussen, F.H. Fluorescent substrates for the proteinases ADAM17, ADAM10, ADAM8, and ADAM12 useful for high-throughput inhibitor screening. Anal. Biochem. 366(2), 144-148 (2007).|3. Mezil, L., Berruyer-Pouyet, C., Cabaud, O., et al. Tumor selective cytotoxic action of a thiomorpholin hydroxamate inhibitor (TMI-1) in breast cancer. PLoS One 7(9), e43409 (2012).
| Cas No. | 287403-39-8 | SDF | |
| 别名 | WAY-171318 | ||
| Canonical SMILES | CC#CCOC1=CC=C(S(N2CCSC(C)(C)[C@@H]2C(NO)=O)(=O)=O)C=C1 | ||
| 分子式 | C17H22N2O5S2 | 分子量 | 398.5 |
| 溶解度 | DMSO: 25 mg/ml | 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 | 2.5094 mL | 12.5471 mL | 25.0941 mL |
| 5 mM | 0.5019 mL | 2.5094 mL | 5.0188 mL |
| 10 mM | 0.2509 mL | 1.2547 mL | 2.5094 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。
Anatomically based radiological classification of thumb basal joint arthritis
Hand Surg Rehabil 2021 Sep;40S:S15-S20.PMID:33373714DOI:10.1016/j.hansur.2020.04.013.
The numerous surgical techniques proposed for treating thumb basal joint arthritis (osteotomy of the first metacarpal, trapezial osteotomy, simple trapeziectomy, trapeziectomy with implant, total joint prosthesis, arthroplasty by interposition, etc.) necessitate an anatomically based radiological evaluation of the different pathological forms of thumb basal joint arthritis. Here, the author defines three parameters: narrowing of the trapeziometacarpal (TM) joint space: TMA; TM instability and subluxation: TM I; scaphotrapeziotrapezoid damage: STT. Four stages of TM osteoarthritic deterioration are defined: TMA0: no joint narrowing (painful and unstable joint); TMA1: narrowing <50%; TMA2: narrowing>50%; TMA3: disappearance of the joint space, bone erosions. For TM instability/subluxation: TMI 0: reducible subluxation (unstable and painful TM); TMI 1: reducible subluxation but with imperfect reintegration; TMI 2: non-reducible subluxation <1/3; TMI 3: subluxation>1/3. For STT damage, STT 0: radiograph is normal but anatomical damage is visible intraoperatively; STT 1: joint space narrowing <50%; STT 2: joint space is barely visible; STT 3: presence of erosion, sclerosis, irregularities. He outlines the shortcomings of the often-used Dell and Eaton-Littler classifications. A prospective study involving multiple cases having the same anatomical and radiological appearance that are assessed with sufficient follow-up is needed to standardize the modalities of surgical treatment.
Among Unstable Angina and Non-ST-Elevation Myocardial Infarction Patients, Transient Myocardial Ischemia and Early Invasive Treatment Are Predictors of Major In-hospital Complications
J Cardiovasc Nurs 2016 Jul-Aug;31(4):E10-9.PMID:26646595DOI:10.1097/JCN.0000000000000310.
Background: Treatment for unstable angina (UA) or non-ST-elevation myocardial infarction (NSTEMI) is aimed at plaque stabilization to prevent infarction. Two treatment strategies are (1) invasive (ie, cardiac catheterization laboratory <24 hours after admission) or (2) selectively invasive (ie, medications with cardiac catheterization laboratory >24 hours for recurrent symptoms). However, it is not known if the frequency of transient myocardial ischemia (TMI) or complications during hospitalization varies by treatment. Purpose: We aimed to (1) examine occurrence of TMI in UA/NSTEMI, (2) compare frequency of TMI by treatment pathway, and (3) determine predictors of in-hospital complications (ie, death, myocardial infarction [MI], pulmonary edema, shock, dysrhythmia with intervention). Methods: Hospitalized patients with coronary artery disease (ie, history of MI, percutaneous coronary intervention/stent, coronary artery bypass graft, >50% lesion via angiogram, or positive troponin) were recruited, and 12-lead electrocardiogram Holter initiated. Clinicians, blinded to Holter data, decided treatment strategy; offline analysis was done after discharge. Transient myocardial ischemia was defined as more than 1-mm ST segment ↑ or ↓, in more than 1 electrocardiographic lead, more than 1 minute. Results: Of 291 patients, 91% were white, 66% were male, 44% had prior MI, and 59% had prior percutaneous coronary intervention/stent or coronary artery bypass graft. Treatment pathway was early in 123 (42%) and selective in 168 (58%). Forty-nine (17%) had TMI: 19 (15%) early invasive, 30 (18%) selective (P = .637). Acute MI after admission was higher in patients with TMI regardless of treatment strategy (early: no TMI 4% vs yes TMI 21%; P = .020; selective: no TMI 1% vs yes TMI 13%; P = .0004). Predictors of major in-hospital complication were TMI (odds ratio, 9.9; 95% confidence interval, 3.84-25.78) and early invasive treatment (odds ratio 3.5; 95% confidence interval, 1.23-10.20). Conclusions: In UA/NSTEMI patients treated with contemporary therapies, TMI is not uncommon. The presence of TMI and early invasive treatment are predictors of major in-hospital complications.
The in vitro development of immunoglobulin producing cells from the human bone marrow null lymphocyte
Tohoku J Exp Med 1981 Mar;133(3):257-66.PMID:7198307DOI:10.1620/tjem.133.257.
The distribution of human bone marrow lymphocyte population was studied on twenty normal adults. The distribution of bone marrow lymphocytes were as follows: null lymphocytes 79.4%, E-RFC 8.9%, Thy+ lymphocytes 0.4%, Tgamma 0.9%, TMI 1.4%, SmIg+ cells 7.8%, EAC-RFC 11.7%, EA-RFC 6.2%, and K cells 2.7%. Bone marrow null lymphocytes were intermediate in their size between small lymphocytes and lymphoblasts. The presence of a lot of short microvilli on null lymphocytes was demonstrated by scanning electron microscopic examinations. The bone marrow null lymphocytes had no cytoplasmic Ig. When the bone marrow null lymphocytes were mixed-lymphocytes-cultured with allogeneic T lymphocytes and then stimulated with PWM, there developed Ig producing cells. Differences between pre-B cells and bone marrow null lymphocytes were discussed.