TNF-α Antagonist - CAS:199999-60-5

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TNF-α Antagonist (Synonyms:WP9QY)

目录号 : KCM12357 CAS No. : 199999-60-5

Data Sheet 产品使用指南

TNF-α antagonist is an exocyclic peptide that mimics the critical TNF-α recognition loop on TNF receptor I complex and, thus, prevents ligand interaction with the receptor. By blocking the TNF receptor ligand contact site, this peptide interferes with both activating receptor activator of NF-κB (RANK) and TNF-α’s recruitment and activation of osteoclasts. TNF-α antagonist has been used to block bone resorption in the study of systemic bone loss in rheumatoid arthritis and inflammatory bone destruction.

规格	价格	是否有货	数量
500μg		In-stock
1mg		In-stock
5mg		In-stock

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生物活性

TNF-α Antagonist is an inhibitor targeting TNFα and RANKL, which blocks the TNFα-TNFR1 interaction and inhibits TNFα-mediated apoptosis, cytotoxicity and bone destruction.

体外研究

TNF - α Antagonist functionalized PEG hydrogel (100-250 μM; 24 h TNF α exposure, 6 d NGF differentiation culture) can protect differentiated PC12 cells from apoptosis induced by 50 ng/mL human TNF α, maintain cell viability and prevent the increase of caspase 3/7 activation level.
TNF - α Antagonist functionalized PEG hydrogel (100 μM; 24h) can protect the embedded mouse islets from apoptosis and insulin secretion damage induced by 50 ng/mL human TNF α, and maintain cell viability and function.
TNF - α Antagonist (10 μM; 72 h) can inhibit neuronal cell death induced by 50 μM methylmercury in vitro in mouse organotypic brain slices.
TNF - α Antagonist (100 μM; 14 d) can significantly enhance cartilage differentiation in hMSC two-dimensional culture system by accumulating glycosaminoglycan matrix, which was confirmed by Alcian Blue staining and absorbance detection.
TNF - α Antagonist (25-100 μM; 72 h) can dose dependently promote the proliferation of hMSCs cultured in maintenance medium, chondrocyte differentiation medium, and osteoblast differentiation medium, as confirmed by Hoechst 33342 fluorescence detection.
TNF - α Antagonist (100 μM; 14 d) can induce chondrocyte differentiation in the control group and RANKL knockdown C3H10T1/2 cells, and is independent of the RANKL signaling pathway.
TNF - α Antagonist (5-50 μM; 20 min) can dose dependently inhibit the RANKL induced signaling pathway in RAW 264.7 cells, without affecting the M-CSF induced signaling pathway.

Cell Viability Assay

Cell Line:	differentiated rat adrenal pheochromocytoma (PC12) cells
Concentration:	100-250 μM WP9QY; 50 ng/mL human TNFα; 50 ng/mL 2.5S NGF
Incubation Time:	24 hours (TNFα exposure); 6 days (NGF differentiation)
Result:	Maintained viability comparable to unchallenged cells in PEG-RGD-WP9QY hydrogels (100 μM and 250 μM WP9QY) under TNFα challenge. Showed no significant increase in caspase 3/7 activity. Confirmed minimal cell death via Live/Dead imaging.

Cell Differentiation Assay

Cell Line:	human mesenchymal stem cells (hMSCs)
Concentration:	100 μM
Incubation Time:	14 days
Result:	Increased absorbance at 620 nm to ~0.27, which was significantly higher than control's ~0.17 with p < 0.01.

体内研究

TNF - α Antagonist (5 mg; intra-articular injection; Twice (on the 14th and 21st day) can significantly improve the repair effect of full-thickness articular cartilage defects in rabbits, manifested as a decrease in the modified Wakitani score.
TNF - α Antagonist (2.1 mg/kg/d; continuously infused through osmotic micro pumps; 4 weeks) can completely prevent osteoporosis induced by ovariectomy in female C57BL/6J mice, restore trabecular bone parameters to sham surgery levels, and reduce osteoclast activity to near sham surgery levels.
TNF - α Antagonist (9 mg/kg; subcutaneous injection; Once every 3 hours; Continuous exposure for 48 hours can completely prevent osteoporosis induced by a low calcium diet in male CD-1 mice, restore trabecular bone parameters to near normal calcium diet levels, and reduce osteoclast activity to near normal calcium diet levels.
TNF - α Antagonist (4 mg/kg/d; continuously infused through osmotic micro pumps; 7 days) can completely prevent osteoporosis induced by low dietary Ca2+in TNFR (I) -/- TNFR (II) -/- mice and wild-type mice.

Animal Model:	Japanese white (male, 19-20 weeks old)
Dosage:	5 mg
Administration:	intraarticular; 2 doses (days 14 and 21)
Result:	Caused partial filling of articular cartilage defects and expanded Safranin-O-positive regions in defects. Reduced mean modified Wakitani score to ~7, versus ~12 for vehicle (P=0.04).

Animal Model:	C57BL/6J Mice (female, 12 weeks old, bilateral ovariectomy-induced)
Dosage:	2.1 mg/kg/d
Administration:	continuous infusion via osmotic minipump; 4 weeks
Result:	Maintained bone mineral density of proximal tibiae at levels not significantly different from sham-operated mice. Restored cancellous bone volume fraction from 9.10% to 14.79%. Restored trabecular number from 6.10 no./mm to 8.01 no./mm. Restored trabecular spacing from 150.12 μm to 109.998 μm. Reduced osteoclast number per bone surface from 7.62 no./mm to 3.65 no./mm. Reduced osteoclast surface per bone surface from 11.58% to 5.96%. Blocked the ovariectomy-induced increase in urinary deoxypyridinoline cross-links. Had no effect on body weight or uterine weight.

分子式

C₅₈H₇₁N₁₁O₁₅S₂

分子量

1226.38

CAS号

199999-60-5

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

2-8°C, protect from light

* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

溶解性数据

In Vitro:

DMSO : 100 mg/mL (81.54 mM; Need ultrasonic)

H2O : 1 mg/mL (0.82 mM; Need ultrasonic)

配制储备液

浓度溶剂体积质量	1 mg	5 mg	10 mg

1 mM	0.8154 mL	4.0770 mL	8.1541 mL
5 mM	0.1631 mL	0.8154 mL	1.6308 mL
10 mM	0.0815 mL	0.4077 mL	0.8154 mL

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, 6 months; -20°C, 1 month (sealed storage, away from moisture)。-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。

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用；以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

1.

请依序添加每种溶剂： 2% DMSO → 10% PEG300 → 2% Tween-80 → 86% Saline

Solubility: ≥ 2 mg/mL (1.63 mM); Clear solution

Data Sheet

产品使用指南

Toyama T, et al. Methylmercury induces neuronal cell death by inducing TNF-α expression through the ASK1/p38 signaling pathway in microglia. Sci Rep. 2021;11(1):9832. Published 2021 May 10.

The molarity calculator equation

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

质量

浓度

体积

分子量*

重置计算

The dilution calculator equation

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
This equation is commonly abbreviated as: C1V1 = C2V2

浓度

体积

浓度

体积

重置计算

动物实验计算换算器

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

每只动物给药体积

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，请联系客服为您提供正确的澄清溶液配方）

% DMSO

% Tween 80

% ddH₂O

% DMSO

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，注：如该浓度超过该批次药物DMSO溶解度，请先联系客服）；

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 ddH₂O，混匀澄清。

配置后的溶液总体积：

注意：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。

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The molarity calculator equation

The dilution calculator equation

动物实验计算换算器