製品番号: HY-118119

CAY10526

2 Cited Publications

カスタマーレビュー

Based on 2 publication(s) in Google Scholar

CAY10526 is an inhibitor of Y-box binding protein 1 (YB-1) and microsomal prostaglandin E2 synthase 1 (mPGES1). CAY10526 inhibits the production of PGE₂ by suppressing YB-1 and mPGES1. CAY10526 induces cell apoptosis (apoptosis) and inhibits the JAK/STAT, TGF-β/Smad3 and PI3K/AKT signaling pathways. CAY10526 can be used in research related to melanoma, prostate cancer, esophageal adenocarcinoma, T-cell lymphoma, etc.

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純度: 99.12%
CAS 番号: 938069-71-7
分子式: C₁₂H₇BrO₃S
分子量:311.16

保管条件:

4°C, sealed storage, away from moisture and light

* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)

CAY10526 構造式

CAS 番号: 938069-71-7

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生物活性
- 製品説明
- Cellular Effect
- 体外実験
- 体内実験
化学情報
Publications (2)
溶剤 & 溶解度
- 体外
- 体内
純度とドキュメンテーション
参考文献
Help & FAQs
関連分類
Bioz

生物活性

製品説明

JAK アイソフォーム固有の製品をすべて表示 :

STAT アイソフォーム固有の製品をすべて表示 :

TGF-β Receptor アイソフォーム固有の製品をすべて表示 :

TGF-beta/Smad アイソフォーム固有の製品をすべて表示 :

Smad1
Smad3

PI3K アイソフォーム固有の製品をすべて表示 :

Akt アイソフォーム固有の製品をすべて表示 :

Cellular Effect

Cell Line	Type	Value	Description	References
A549	IC₅₀	>10 μM Compound: 1	Inhibition of mPGES-1-mediated PGE2 formation in IL-1beta-stimulated human A549 cells preincubated for 10 mins measured after 1 min by RP-HPLC analysis Inhibition of mPGES-1-mediated PGE2 formation in IL-1beta-stimulated human A549 cells preincubated for 10 mins measured after 1 min by RP-HPLC analysis	[PMID: 22795900]
A549	IC₅₀	12.5 μM Compound: CAY10526	Antiproliferative activity against human A549 cells assessed as inhibition of cell viability incubated for 48 hrs by MTT assay Antiproliferative activity against human A549 cells assessed as inhibition of cell viability incubated for 48 hrs by MTT assay	[PMID: 32435385]
A549	IC₅₀	9.1 μM Compound: CAY10526	Antiproliferative activity against human A549 cells assessed as inhibition of cell viability incubated for 72 hrs by MTT assay Antiproliferative activity against human A549 cells assessed as inhibition of cell viability incubated for 72 hrs by MTT assay	[PMID: 32435385]
A549	IC₅₀	98.5 μM Compound: CAY10526	Antiproliferative activity against human A549 cells assessed as inhibition of cell viability incubated for 24 hrs by MTT assay Antiproliferative activity against human A549 cells assessed as inhibition of cell viability incubated for 24 hrs by MTT assay	[PMID: 32435385]
RAW264.7	IC₅₀	1.8 μM Compound: 4e	Inhibition of PGE2 production in LPS-stimulated mouse RAW264.7 cells after 18 hrs Inhibition of PGE2 production in LPS-stimulated mouse RAW264.7 cells after 18 hrs	[PMID: 17407277]
RAW264.7	IC₅₀	1.8 μM Compound: 34	Inhibition of lipopolysaccharide-stimulated PGE2 production in mouse RAW264.7 cells Inhibition of lipopolysaccharide-stimulated PGE2 production in mouse RAW264.7 cells	[PMID: 18459759]

体外実験

CAY10526 (5 μM; 1 h) potently inhibits NO donor-induced PGE₂ production in human melanoma cell lines A375 and SB2^[1].
CAY10526 (0-20 μM; 72 h) potently reduces the viability of human melanoma cell lines A375, SB2 and WM793 with high mPGES1 expression, with an IC₅₀ < 5 μM; whereas in human melanoma cell lines SK-MEL-28, WM1361A with low mPGES1 expression and BJ fibroblasts, the activity of this compound is significantly attenuated (IC₅₀ >10 μM)^[1].
CAY10526 (5 μM; 48 h) regulates 69 proteins associated with cell death and survival, including reducing the phosphorylation level of YB-1, cyclin B1, and the anti-apoptotic proteins BCL-2/BCL-XL, while upregulating p21, the pro-apoptotic proteins BAX/BAK, and activated caspase-3 in A375 and SB2 human melanoma cells^[1].
CAY10526 (1-50 μM; 12 h) inhibits the proliferation of DU-145 prostate cancer cells in a concentration-dependent manner. A significant reduction in cell viability is observed at concentrations of 10 μM and 20 μM, and the inhibitory effect reaches a plateau when the concentration exceeds 20 μM^[2].
CAY10526 (10-20 μM; 12 h) downregulates mPGES-1 expression in DU-145 prostate cancer cells in a concentration-dependent manner in vitro; at a concentration of 10 μM, it maintains high expression levels of Beclin-1 compared with the complete medium control group, while at 20 μM, it significantly reduces the expression of both mPGES-1 and Beclin-1^[2].
CAY10526 (1-50 μM; 18 h) potently inhibits leptin-induced PGE₂ production in OE33 esophageal adenocarcinoma cells, achieving complete inhibition at concentrations of 10 μM and 50 μM^[4].
CAY10526 (10 μM; 18 h) inhibits leptin-induced mPGES-1 protein expression in OE33 esophageal adenocarcinoma cells without altering COX-2 expression^[4].
CAY10526 (1-50 μM; 24 h) inhibits leptin-induced proliferation in OE33 esophageal adenocarcinoma cells in a concentration-dependent manner, reaching maximum inhibitory activity at 10 μM and 50 μM, which is comparable to the activity of active COX-2 inhibitors at corresponding concentrations^[4].
CAY10526 (1-50 μM; 48 h) reduces the number of viable serum-cultured OE33 esophageal adenocarcinoma cells in a concentration-dependent manner, with maximal activity observed at 10 μM^[4].
CAY10526 (1-50 μM; 25 h) inhibits leptin-induced increase in the number of viable OE33 esophageal adenocarcinoma cells in a concentration-dependent manner, with its maximal activity achieved at 10 μM^[4].
CAY10526 (10 μM; 25 h) inhibits leptin-induced proliferation in OE33 esophageal adenocarcinoma cells by targeting the upstream pathway of PGE₂ production, while exogenous PGE₂ restores this proliferative effect^[4].
CAY10526 (10 μM; 25 h) inhibits IL-1β-induced PGE₂ production and promotes PGI₂ production in HUVECs, without affecting endothelial prostacyclin synthesis^[4].
CAY10526 (25 h) inhibits thrombin-induced PGE₂ production and promotes PGI₂ production in human umbilical vein endothelial cells (HUVECs), without affecting endothelial prostacyclin synthesis^[4].
CAY10526 (10-80 μM; 24-72 h) inhibits the proliferation of human T-cell lymphoma Hut78 cells, with an IC₅₀ of 27.64 μM at 24 h, and suppresses cell viability in a dose-dependent manner after 72 h of incubation^[5].
CAY10526 (10-80 μM; 24 h) reduces the expression of mPGES-1 protein in human T-cell lymphoma Hut78 cells in a dose-dependent manner, and exerts significant inhibitory effects at concentrations of 40 μM and 80 μM after 24 h^[5].
CAY10526 (10-80 μM; 24 h) inhibits PGE₂ synthesis in human T-cell lymphoma Hut78 cells in a dose-dependent manner, and exerts significant inhibitory effects at concentrations of 10, 20, 40 and 80 μM after 24 h^[5].
CAY10526 (20-40 μM; 24 h) induces apoptosis in human T-cell lymphoma Hut78 cells in a dose-dependent manner, and the apoptosis rates at concentrations of 20 μM and 40 μM increase significantly after 24 h^[5].
CAY10526 (20-40 μM; 24 h) upregulates the expression of activated caspase-3 in human T-cell lymphoma Hut78 cells in a dose-dependent manner, and the expression levels at 20 μM and 40 μM increase significantly after 24 h^[5].
CAY10526 (20-40 μM; 24 h) dose-dependently inhibits the JAK/STAT signaling pathway in human T-cell lymphoma Hut78 cells by reducing the expression of JAK1, JAK2 and p-STAT3; after 24 h, the inhibitory effect is significant at concentrations of 20 μM and 40 μM, while the total STAT3 level remains unchanged^[5].
CAY10526 (20-40 μM; 24 h) dose-dependently inhibits the PI3K/AKT signaling pathway in human T-cell lymphoma Hut78 cells by reducing the expression of PI3Kp110, PI3Kp85 and p-AKT; after 24 h of treatment, the inhibitory effect is significant at concentrations of 20 μM and 40 μM, while the total AKT level remains unchanged^[5].
CAY10526 (20-40 μM; 24 h) inhibits the TGF-β/Smad3 signaling pathway in human T-cell lymphoma Hut78 cells in a dose-dependent manner by reducing the expression of TGF-β and p-Smad3; after 24 h of treatment, the inhibitory effect is significant at concentrations of 20 μM and 40 μM, while the total Smad3 level remains unchanged^[5].
CAY10526 (20-40 μM; 24 h) reduces CyclinD1 expression in human T-cell lymphoma Hut78 cells in a dose-dependent manner, and exerts significant inhibitory effects at concentrations of 20 μM and 40 μM after 24 h^[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Viability Assay^[1]

Cell Line:

A375, SB2, WM793, SK-MEL-28, WM1361A human melanoma cells, BJ normal fibroblasts
Concentration:

0, 1, 5, 10 and 20 μM
Incubation Time:

72 h
Result:

Inhibited cell viability with an IC₅₀ < 5 μM in mPGES1-high melanoma cell lines (A375, SB2, WM793).
Showed significantly weaker activity with an IC₅₀ >10 μM in mPGES1-low melanoma cell lines (SK-MEL-28, WM1361A) and normal BJ fibroblasts.

Cell Proliferation Assay^[2]

Cell Line:

DU-145 prostate cancer cells
Concentration:

1, 10, 20 and 50 μM
Incubation Time:

12 h
Result:

Inhibited DU-145 cell proliferation in a concentration-dependent manner.
Exhibited optical density values of 0.34 at 1 μM, 0.22 at 10 μM, 0.08 at 20 μM, and 0.06 at 50 μM.
Reduced cell viability significantly at 10 μM and 20 μM compared to control.
Showed no significant difference in cell viability between 20 μM and 50 μM groups.

Western Blot Analysis^[2]

Cell Line:

DU-145 prostate cancer cells
Concentration:

10 and 20 μM
Incubation Time:

12 h (serum-free conditions)
Result:

Downregulated mPGES-1 protein expression in a concentration-dependent manner.
Reduced Beclin-1 expression at 10 μM compared to serum-free group, while levels remained higher than complete medium control group.
Significantly downregulated both mPGES-1 and Beclin-1 at 20 μM.

ELISA Assay^[4]

Cell Line:

leptin-stimulated OE33 oesophageal adenocarcinoma cells
Concentration:

1 μM, 10 μM, 50 μM
Incubation Time:

60 min pretreatment, followed by 18 h leptin stimulation
Result:

Caused a concentration-dependent reduction in leptin-driven, COX-2-dependent PGE2 production.
Abolished leptin-induced PGE2 production at 10 μM and 50 μM, achieving inhibition comparable to COX-2 inhibitors celecoxib and NS-398 at their active concentrations.

Western Blot Analysis^[4]

Cell Line:

leptin-stimulated OE33 oesophageal adenocarcinoma cells
Concentration:

10 μM
Incubation Time:

60 min pretreatment, followed by 18 h leptin stimulation
Result:

Completely blocked leptin-induced mPGES-1 protein expression.
Left COX-2 protein expression unaffected.

Cell Proliferation Assay^[4]

Cell Line:

leptin-stimulated OE33 oesophageal adenocarcinoma cells
Concentration:

1 μM, 10 μM, 50 μM
Incubation Time:

60 min pretreatment, followed by 24 h leptin stimulation
Result:

Caused a concentration-dependent decrease in leptin-stimulated OE33 cell proliferation.
Blocked leptin-induced proliferation at 10 μM and 50 μM with effectiveness matching COX-2 inhibitors celecoxib (1 μM) and NS-398 (10 μM).

Cell Viability Assay^[4]

Cell Line:

serum-cultured OE33 oesophageal adenocarcinoma cells
Concentration:

1 μM, 10 μM, 50 μM
Incubation Time:

48 h
Result:

Caused a concentration-dependent reduction in viable OE33 cell numbers, with no further reduction observed at concentrations above 10 μM.
Significantly reduced viable cell numbers at all tested concentrations compared to untreated controls.

Cell Viability Assay^[4]

Cell Line:

leptin-stimulated OE33 oesophageal adenocarcinoma cells
Concentration:

1 μM, 10 μM, 50 μM
Incubation Time:

60 min pretreatment, followed by 24 h leptin stimulation
Result:

Blunted the leptin-stimulated increase in viable OE33 cell numbers in a concentration-dependent manner, with no additional effect observed at concentrations above 10 μM.
Significantly reduced leptin-stimulated viable cell numbers at all tested concentrations compared to leptin-only controls.

Cell Viability Assay^[4]

Cell Line:

leptin-stimulated OE33 oesophageal adenocarcinoma cells (PGE2-rescue experiment)
Concentration:

10 μM
Incubation Time:

60 min pretreatment, followed by 24 h stimulation with leptin, PGE2, or leptin + PGE2
Result:

Allowed exogenous PGE2 to stimulate OE33 cell proliferation even in its presence.
Saw the inhibitory effect on leptin-stimulated proliferation reversed by added PGE2.

ELISA Assay^[4]

Cell Line:

IL-1β-stimulated human umbilical vein endothelial cells (HUVECs)
Concentration:

10 μM
Incubation Time:

60 min pretreatment, followed by 24 h IL-1β stimulation
Result:

Effectively blocked IL-1β-driven PGE2 production in HUVECs.
Significantly enhanced IL-1β-stimulated PGI2 production, unlike COX-2 inhibitors celecoxib and NS-398 which abolished production of both PGE2 and PGI2.

ELISA Assay^[4]

Cell Line:

thrombin-stimulated human umbilical vein endothelial cells (HUVECs)
Concentration:

10 μM
Incubation Time:

60 min pretreatment, followed by 24 h thrombin stimulation
Result:

Blocked thrombin-stimulated PGE2 production in HUVECs.
Significantly enhanced thrombin-stimulated PGI2 production, unlike COX-2 inhibitors celecoxib and NS-398 which abolished production of both PGE2 and PGI2.

Western Blot Analysis^[5]

Cell Line:

human T-cell lymphoma Hut78 cells
Concentration:

10, 20, 40 and 80 μM
Incubation Time:

24 h
Result:

Down-regulated mPGES-1 protein expression in Hut78 cells in a dose-dependent manner.
Caused statistically significant reductions at 40 μM and 80 μM compared to untreated cells.

Apoptosis Analysis^[5]

Cell Line:

human T-cell lymphoma Hut78 cells
Concentration:

20 and 40 μM
Incubation Time:

24 h
Result:

Significantly increased the apoptosis rate of Hut78 cells in a dose-dependent manner.
Caused statistically significant elevations at 20 μM and 40 μM compared to untreated cells.

Western Blot Analysis^[5]

Cell Line:

human T-cell lymphoma Hut78 cells
Concentration:

20 and 40 μM
Incubation Time:

24 h
Result:

Increased the expression of cleaved caspase-3 in Hut78 cells in a dose-dependent manner.
Caused statistically significant elevations at 20 μM and 40 μM compared to untreated cells.\nDecreased the expression of JAK1, JAK2, and p-STAT3 in Hut78 cells in a dose-dependent manner.
Caused statistically significant reductions at 20 μM and 40 μM compared to untreated cells.
Left total STAT3 expression unchanged.\nDecreased the expression of PI3Kp110, PI3Kp85, and p-AKT in Hut78 cells in a dose-dependent manner.
Caused statistically significant reductions at 20 μM and 40 μM compared to untreated cells.
Left total AKT expression unchanged.\nDecreased the expression of TGF-β and p-Smad3 in Hut78 cells in a dose-dependent manner.
Caused statistically significant reductions at 20 μM and 40 μM compared to untreated cells.
Left total Smad3 expression unchanged.\nDecreased CyclinD1 expression in Hut78 cells in a dose-dependent manner.
Caused statistically significant reductions at 20 μM and 40 μM compared to untreated cells.

体内実験

CAY10526 (25-50 mg/kg; i.p.; daily; 15 days) reduces melanoma xenograft tumor volume by 43% and tumor weight by 48%, while decreasing p-YB-1 levels and increasing cleaved caspase 3 levels in tumor tissue^[1].
CAY10526 (2.5 mg/kg; i.p.; daily; 7 days) either during obstruction or starting at obstruction release normalizes PGE₂ levels and improves or restores colon motility and smooth muscle contractility in post-BO rats^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

athymic nu/nu (male, 6-8 weeks old, subcutaneous xenograft model)^[1]
Dosage:

25 mg/kg; 50 mg/kg
Administration:

i.p.; daily; 15 days
Result:

Reduced tumor volume by 43% and tumor weight by 48% relative to vehicle controls at 50 mg/kg dose.
Decreased phosphorylation of Y-box binding protein 1 (p-YB-1) and increased levels of cleaved caspase 3 in tumor tissues at 50 mg/kg dose.

Animal Model:

Sprague-Dawley (male, 225-275 g, partial colon obstruction induced with obstruction band, released after 7 days to create post-bowel obstruction state)^[3]
Dosage:

2.5 mg/kg (starting on obstruction release); 2.5 mg/kg (during obstruction period)
Administration:

i.p.; daily; 7 days (starting on obstruction release); i.p.; daily; 7 days (during obstruction period)
Result:

Normalized PGE₂ levels in colonic muscularis externae.
Eliminated the difference in colon transit geometric center between post-BO and post-sham rats.
Restored colonic circular smooth muscle contractility in response to acetylcholine to post-sham levels.
Partially but significantly improved colonic circular smooth muscle contractility in response to acetylcholine in the post-BO state.

化学情報

CAS 番号 938069-71-7
性状 Solid
分子量 311.16
分子式 C₁₂H₇BrO₃S
Color Off-white to yellow
SMILES

O=C1C(Br)=C(C(O1)O)C2=CC3=CC=CC=C3S2
輸送条件

Room temperature in continental US; may vary elsewhere.
保管条件

4°C, sealed storage, away from moisture and light

* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)

Publications (2)

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Signal Transduct Target Ther

Prostaglandin E2-driven dedifferentiation of Schwann cells leads to perineural invasion in pancreatic ductal adenocarcinoma. [Abstract]

2026 Apr 7;11(1):122. PMID: 41946682
Genes Immun

MTA1-mediated transcriptional repression of Cox2 confers resistance against neutrophil infiltration in endometritis. [Abstract]

2026 Mar 10. PMID: 41807815

溶剤 & 溶解度

体外:

DMSO : 66.67 mg/mL (214.26 mM; ultrasonic and warming and heat to 60°C; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

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Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

3.2138 mL

16.0689 mL

32.1378 mL

5 mM

0.6428 mL

3.2138 mL

6.4276 mL

10 mM

0.3214 mL

1.6069 mL

3.2138 mL

Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.

Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

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体内:

Select the appropriate dissolution method based on your experimental animal and administration route.

Stock Solution Working Solution

For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

Protocol 1

Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)

Solubility: 2.5 mg/mL (8.03 mM); Clear solution; Need ultrasonic

This protocol yields a clear solution of 2.5 mg/mL.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

In Vivo Dissolution Calculator

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The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).

Working solution concentration: 0.22 mg/mL

純度とドキュメンテーション

バッチを選択:

純度: 99.98%

Assay: 99.98%

ee.: 99.98%

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参考文献

[1]. Kim SH, et al. Microsomal PGE2 synthase-1 regulates melanoma cell survival and associates with melanoma disease progression. Pigment Cell Melanoma Res. 2016 May;29(3):297-308.
[Content Brief]

[2]. Xu LW, et al. Expression and significance of microsomal prostaglandin synthase-1 (mPGES-1) and Beclin-1 in the development of prostate cancer. Asian Pac J Cancer Prev. 2012;13(4):1639-1644. [Content Brief]

[3]. Lin YM, et al. Microsomal Prostaglandin E Synthase-1 Plays a Critical Role in Long-term Motility Dysfunction after Bowel Obstruction. Sci Rep. 2018;8(1):8831. Published 2018 Jun 11. [Content Brief]

[4]. Beales IL, et al. Microsomal prostaglandin E synthase-1 inhibition blocks proliferation and enhances apoptosis in oesophageal adenocarcinoma cells without affecting endothelial prostacyclin production. Int J Cancer. 2010;126(9):2247-2255. [Content Brief]

[5]. Li Y, et al. Growth of T-cell lymphoma cells is inhibited by mPGES-1/PGE2 suppression via JAK/STAT, TGF-β/Smad3 and PI3K/AKT signal pathways. Transl Cancer Res. 2022;11(7):2175-2184. [Content Brief]

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	3.2138 mL	16.0689 mL	32.1378 mL	80.3445 mL
	5 mM	0.6428 mL	3.2138 mL	6.4276 mL	16.0689 mL
	10 mM	0.3214 mL	1.6069 mL	3.2138 mL	8.0345 mL
	15 mM	0.2143 mL	1.0713 mL	2.1425 mL	5.3563 mL
	20 mM	0.1607 mL	0.8034 mL	1.6069 mL	4.0172 mL
	25 mM	0.1286 mL	0.6428 mL	1.2855 mL	3.2138 mL
	30 mM	0.1071 mL	0.5356 mL	1.0713 mL	2.6782 mL
	40 mM	0.0803 mL	0.4017 mL	0.8034 mL	2.0086 mL
	50 mM	0.0643 mL	0.3214 mL	0.6428 mL	1.6069 mL
	60 mM	0.0536 mL	0.2678 mL	0.5356 mL	1.3391 mL
	80 mM	0.0402 mL	0.2009 mL	0.4017 mL	1.0043 mL
	100 mM	0.0321 mL	0.1607 mL	0.3214 mL	0.8034 mL

CAY10526

2 Cited Publications

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CAY10526

Apoptosis Compound Library

Cell Cycle/DNA Damage Compound Library

Epigenetics Compound Library

Immunology/Inflammation Compound Library

JAK/STAT Compound Library

Kinase Inhibitor Library

PI3K/Akt/mTOR Compound Library

Protein Tyrosine Kinase Compound Library

Stem Cell Signaling Compound Library

TGF-beta/Smad Compound Library

Wnt/Hedgehog/Notch Compound Library

Anti-Cancer Compound Library

Autophagy Compound Library

Anti-Aging Compound Library

Differentiation Inducing Compound Library

Reprogramming Compound Library

Oxygen Sensing Compound Library

Glycolysis Compound Library

Pyroptosis Compound Library

Cytoskeleton Compound Library

Glutamine Metabolism Compound Library

Anti-Breast Cancer Compound Library

Anti-Lung Cancer Compound Library

Anti-Pancreatic Cancer Compound Library

Anti-Blood Cancer Compound Library

Anti-Cancer Metabolism Compound Library

Anti-Obesity Compound Library

Angiogenesis-Related Compound Library

Transcription Factor-Targeted Library

Glucose Metabolism Compound Library

Anti-Liver Cancer Compound Library

Anti-Colorectal Cancer Compound Library

Anti-Prostate Cancer Compound Library

Anti-Pulmonary Fibrosis Compound Library

Osteogenesis Compound Library

Cancer Stem Cells Compound Library

Heterocyclic Compound Library

Pain-Related Compound Library

Membrane Protein-targeted Compound Library

Membrane Receptor-targeted Compound Library

Autoimmune Disease Compound Library

Cytokine Inhibitors Library

Cell Death Library

Serine/Threonine Kinase Inhibitor Library

Anti-Hematopathy Compound Library

Anti-Ovarian Cancer Compound Library

Multi-Target Compound Library

Bioactive Compound Library Max

MCE Bioactive Compound Library

Bioactive Compound Library

Anti-Gastric Cancer Compound Library

Anti-Fibrosis Compound Library

Anti-Brain Cancer Compound Library

Protein Kinase Compound Library

Non-Alcoholic Fatty Liver Disease (NAFLD) Compound Library

Cell Proliferation Compound Library

High-Throughput Bioactive Compound Library

Anti-Rheumatic Arthritis Compound Library

Lactylation Compound Library

MedChemExpress（MCE）の使用を引用している文献 CAY10526

JAK アイソフォーム固有の製品をすべて表示

STAT アイソフォーム固有の製品をすべて表示

TGF-β Receptor アイソフォーム固有の製品をすべて表示

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CAY10526 関連分類

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