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Pathways Recommended:	Membrane Transporter/Ion Channel

Results for "

Chloride Channel/COX Inhibitor

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Calcium Channel (5) Chloride Channel (6) COX (10) Potassium Channel (6) Sodium Channel (2) Adrenergic Receptor (2) AMPK (4) Amyloid-β (2) Apoptosis (2) Endogenous Metabolite (3) GlyT (1) iGluR (2) Isotope-Labeled Compounds (3) NF-κB (2) p38 MAPK (2) Parasite (4) Reference Standards (5)
By Research Areas:	Cancer (5) Endocrinology (2) Inflammation/Immunology (11) Neurological Disease (4)

Inhibitors & Agonists

Natural
Products

Isotope-Labeled Compounds

Targets Recommended: Chloride Channel COX Calcium Channel HCN Channel CRAC Channel TRP Channel Sodium Channel Potassium Channel Piezo Channel

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-B1221

Flufenamic acid Maximum Cited Publications 8 Publications Verification	COX AMPK Potassium Channel Chloride Channel Calcium Channel Parasite	Inflammation/Immunology
Flufenamic acid is a non-steroidal anti-inflammatory agent, inhibits cyclooxygenase (COX), activates AMPK, and also modulates ion channels, blocking chloride channels and L-type Ca ²⁺ channels, modulating non-selective cation channels (NSC), activating K ⁺ channels. Flufenamic acid binds to the central pocket of TEAD2 YBD and inhibits both TEAD function and TEAD-YAP-dependent processes, such as cell migration and proliferation.

HY-B1221S1

Flufenamic acid-13C6	Isotope-Labeled Compounds COX AMPK Potassium Channel Chloride Channel Calcium Channel Parasite	Inflammation/Immunology
Flufenamic acid- ¹³C₆ is the ¹³C₆ labeled Flufenamic acid. Flufenamic acid is a non-steroidal anti-inflammatory agent, inhibits cyclooxygenase (COX), activates AMPK, and also modulates ion channels, blocking chloride channels and L-type Ca ²⁺ channels, modulating non-selective cation channels (NSC), activating K+ channels. Flufenamic acid binds to the central pocket of TEAD2 YBD and inhibits both TEAD function and TEAD-YAP-dependent processes, such as cell migration and proliferation.

HY-N0603

20(S)-Ginsenoside Rg3 5 Publications Verification 20(S)-Propanaxadiol; S-ginsenoside Rg3	Sodium Channel Potassium Channel NF-κB COX Amyloid-β Endogenous Metabolite	Neurological Disease Inflammation/Immunology Cancer
20(S)-Ginsenoside Rg3 is the main component of Panax ginseng C. A. Meyer. Ginsenoside Rg3 inhibits Na ⁺ and hKv1.4 channel with IC₅₀s of 32.2±4.5 and 32.6±2.2 μM, respectively. 20(S)-Ginsenoside Rg3 also inhibits Aβ levels, NF-κB activity, and *COX-2* expression.

HY-N2072

Crocetin 1 Publications Verification Transcrocetin; trans-Crocetin	iGluR Apoptosis COX p38 MAPK	Neurological Disease Inflammation/Immunology Cancer
Crocetin (Transcrocetin) is an aglycone of crocin. Crocetin is an orally active and brain-penetrant. Crocetin shows strong NMDA receptor affinity and channel opening activity. Crocetin can downregulate the proinflammatory cytokines and COX-2 exoression. Crocetin can inhibit apoptosis and activation of MAPK. Crocetin can delay delays brain and body aging. Crocetin can be used for the researches of cancer, neurological disease and inflammation, such as cervical cancer and ischemia .

HY-B0493

Niflumic acid 2 Publications Verification	Chloride Channel COX	Inflammation/Immunology Cancer
Niflumic acid is a calcium-activated chloride channel blocker and *COX-2 inhibitor* with the IC₅₀ value of 100 nM. Niflumic acid induces apoptosis through caspase-8/Bid/Bax pathway in lung cancer cells. Niflumic acide exhibits anti-tumor activity by affecting the expression of ERK1/2 and the activity of MMP2 and MMP9. Niflumic acid has orally bioactivity. Niflumic acid acts on rheumatoid arthritis .

HY-N2072R

Crocetin (Standard) Transcrocetin (Standard); trans-Crocetin (Standard)	iGluR Reference Standards Apoptosis COX p38 MAPK	Neurological Disease Inflammation/Immunology Cancer
Crocetin (Standard) (TransCrocetin (Standard) ) is an aglycone of crocin. Crocetin (Standard) is orally active and brain-penetrant. Crocetin (Standard) shows strong NMDA receptor affinity and channel opening activity. Crocetin (Standard) can downregulate the proinflammatory cytokines and COX-2 exoression. Crocetin (Standard) can inhibit apoptosis and activation of MAPK. Crocetin (Standard) can delay delays brain and body aging. Crocetin (Standard) can be used for the researches of cancer, neurological disease and inflammation, such as cervical cancer and ischemia .

HY-B1221R

Flufenamic acid (Standard)	Reference Standards COX AMPK Potassium Channel Chloride Channel Calcium Channel Parasite	Inflammation/Immunology
Flufenamic acid (Standard) is the analytical standard of Flufenamic acid. This product is intended for research and analytical applications. Flufenamic acid is a non-steroidal anti-inflammatory agent, inhibits cyclooxygenase (COX), activates AMPK, and also modulates ion channels, blocking chloride channels and L-type Ca ²⁺ channels, modulating non-selective cation channels (NSC), activating K ⁺ channels. Flufenamic acid binds to the central pocket of TEAD2 YBD and inhibits both TEAD function and TEAD-YAP-dependent processes, such as cell migration and proliferation.

HY-B1221S

Flufenamic acid-d4	Isotope-Labeled Compounds COX AMPK Potassium Channel Chloride Channel Calcium Channel Parasite	Inflammation/Immunology
Flufenamic acid-d₄ is deuterium labeled Flufenamic acid. Flufenamic acid is a non-steroidal anti-inflammatory agent, inhibits cyclooxygenase (COX), activates AMPK, and also modulates ion channels, blocking chloride channels and L-type Ca ²⁺ channels, modulating non-selective cation channels (NSC), activating K+ channels. Flufenamic acid binds to the central pocket of TEAD2 YBD and inhibits both TEAD function and TEAD-YAP-dependent processes, such as cell migration and proliferation.

HY-N0603R

20(S)-Ginsenoside Rg3 (Standard) 20(S)-Propanaxadiol(Standard); S-ginsenoside Rg3 (Standard)	Reference Standards Sodium Channel Potassium Channel NF-κB COX Amyloid-β Endogenous Metabolite	Neurological Disease Inflammation/Immunology Cancer
20(S)-Ginsenoside Rg3 (Standard) is the analytical standard of 20(S)-Ginsenoside Rg3. This product is intended for research and analytical applications. 20(S)-Ginsenoside Rg3 is the main component of Panax ginseng C. A. Meyer. Ginsenoside Rg3 inhibits Na+ and hKv1.4 channel with IC50s of 32.2±4.5 and 32.6±2.2 μM, respectively. 20(S)-Ginsenoside Rg3 also inhibits Aβ levels, NF-κB activity, and COX-2 expression.

HY-103332R

N-Arachidonylglycine (Standard) NA-Gly (Standard)	Reference Standards GlyT Endogenous Metabolite	Inflammation/Immunology
20(S)-Ginsenoside Rg3 (Standard) is the analytical standard of 20(S)-Ginsenoside Rg3. This product is intended for research and analytical applications. 20(S)-Ginsenoside Rg3 is the main component of Panax ginseng C. A. Meyer. Ginsenoside Rg3 inhibits Na+ and hKv1.4 channel with IC50s of 32.2±4.5 and 32.6±2.2 μM, respectively. 20(S)-Ginsenoside Rg3 also inhibits Aβ levels, NF-κB activity, and COX-2 expression.

HY-B0493R

Niflumic acid (Standard)	Reference Standards Chloride Channel COX	Inflammation/Immunology
Niflumic acid (Standard) is the analytical standard of Niflumic acid. This product is intended for research and analytical applications. Niflumic acid is a calcium-activated chloride channel blocker and *COX-2 inhibitor* with the IC₅₀ value of 100 nM. Niflumic acid induces apoptosis through caspase-8/Bid/Bax pathway in lung cancer cells. Niflumic acide exhibits anti-tumor activity by affecting the expression of ERK1/2 and the activity of MMP2 and MMP9. Niflumic acid has orally bioactivity. Niflumic acid acts on rheumatoid arthritis .

HY-132184

5,6-Epoxyeicosatrienoic acid 5,6-EET; (±)5,6-EpETrE	Adrenergic Receptor Calcium Channel	Endocrinology
5,6-Epoxyeicosatrienoic acid (5,6-EET; (±)5,6-EpETrE) is a fully racemic version of the enantiomeric forms biosynthesized from arachidonic acid by cytochrome P450 enzymes. In solution, 5,6-Epoxyeicosatrienoic acid degrades into 5,6-DiHET and 5,6-δ-lactone, which can be converted to 5,6-DiHET and quantified by GC-MS. In neuroendocrine cells, such as the anterior pituitary and pancreatic islets, 5,6-Epoxyeicosatrienoic acid has been implicated in the mobilization of calcium and hormone secretion. 5,6-Epoxyeicosatrienoic acid is an inhibitor of T-type voltage-gated calcium channels (Cav3) that inhibits isoforms Cav3.1, Cav3.2 (IC₅₀=0.54 μM), and Cav3. and decreases nifedipine-resistant phenylephrine-induced vasoconstriction in isolated mouse mesenteric arteries via Cav3.2 blockade when used at a concentration of 3 μM. In addition, it is a substrate of COX-1 and COX-2.

HY-132184S

5,6-Epoxyeicosatrienoic acid-d11 5,6-EET-d₁₁; (±)5,6-EpETrE-d₁₁	Isotope-Labeled Compounds Adrenergic Receptor	Endocrinology
5,6-Epoxyeicosatrienoic acid-d₁₁ (5,6-EET-d₁₁) is deuterium labeled 5,6-Epoxyeicosatrienoic acid. 5,6-Epoxyeicosatrienoic acid (5,6-EET; (±)5,6-EpETrE) is a fully racemic version of the enantiomeric forms biosynthesized from arachidonic acid by cytochrome P450 enzymes. In solution, 5,6-Epoxyeicosatrienoic acid degrades into 5,6-DiHET and 5,6-δ-lactone, which can be converted to 5,6-DiHET and quantified by GC-MS. In neuroendocrine cells, such as the anterior pituitary and pancreatic islets, 5,6-Epoxyeicosatrienoic acid has been implicated in the mobilization of calcium and hormone secretion. 5,6-Epoxyeicosatrienoic acid is an inhibitor of T-type voltage-gated calcium channels (Cav3) that inhibits isoforms Cav3.1, Cav3.2 (IC₅₀=0.54 μM), and Cav3. and decreases nifedipine-resistant phenylephrine-induced vasoconstriction in isolated mouse mesenteric arteries via Cav3.2 blockade when used at a concentration of 3 μM. In addition, it is a substrate of COX-1 and COX-2, as measured by oxygen consumption and product formation assays when used at a concentration of 50 μM. (±)5,6-Epoxyeicosatrienoic acid is provided as a mixture of the free acid and lactone .

Cat. No.	Product Name	Category	Target	Chemical Structure

HY-N0603

20(S)-Ginsenoside Rg3 5 Publications Verification 20(S)-Propanaxadiol; S-ginsenoside Rg3	Panax ginseng C. A. Meyer Triterpenes Neurological Disease Classification of Application Fields Terpenoids Source classification Plants Endogenous metabolite Inflammation/Immunology Disease Research Fields Araliaceae	Sodium Channel Potassium Channel NF-κB COX Amyloid-β Endogenous Metabolite
20(S)-Ginsenoside Rg3 is the main component of Panax ginseng C. A. Meyer. Ginsenoside Rg3 inhibits Na ⁺ and hKv1.4 channel with IC₅₀s of 32.2±4.5 and 32.6±2.2 μM, respectively. 20(S)-Ginsenoside Rg3 also inhibits Aβ levels, NF-κB activity, and *COX-2* expression.

HY-N2072

Crocetin 1 Publications Verification Transcrocetin; trans-Crocetin	Classification of Application Fields Terpenoids Source classification Diterpenoids Lridaceae Plants Crocus sativus L. Endogenous metabolite Disease Research Fields Cancer	iGluR Apoptosis COX p38 MAPK
Crocetin (Transcrocetin) is an aglycone of crocin. Crocetin is an orally active and brain-penetrant. Crocetin shows strong NMDA receptor affinity and channel opening activity. Crocetin can downregulate the proinflammatory cytokines and COX-2 exoression. Crocetin can inhibit apoptosis and activation of MAPK. Crocetin can delay delays brain and body aging. Crocetin can be used for the researches of cancer, neurological disease and inflammation, such as cervical cancer and ischemia .

HY-N2072R

Crocetin (Standard) Transcrocetin (Standard); trans-Crocetin (Standard)	Terpenoids Source classification Diterpenoids Lridaceae Plants Crocus sativus L. Endogenous metabolite	iGluR Reference Standards Apoptosis COX p38 MAPK
Crocetin (Standard) (TransCrocetin (Standard) ) is an aglycone of crocin. Crocetin (Standard) is orally active and brain-penetrant. Crocetin (Standard) shows strong NMDA receptor affinity and channel opening activity. Crocetin (Standard) can downregulate the proinflammatory cytokines and COX-2 exoression. Crocetin (Standard) can inhibit apoptosis and activation of MAPK. Crocetin (Standard) can delay delays brain and body aging. Crocetin (Standard) can be used for the researches of cancer, neurological disease and inflammation, such as cervical cancer and ischemia .

HY-N0603R

20(S)-Ginsenoside Rg3 (Standard) 20(S)-Propanaxadiol(Standard); S-ginsenoside Rg3 (Standard)	Panax ginseng C. A. Meyer Triterpenes Neurological Disease Classification of Application Fields Terpenoids Source classification Plants Endogenous metabolite Inflammation/Immunology Disease Research Fields Araliaceae	Reference Standards Sodium Channel Potassium Channel NF-κB COX Amyloid-β Endogenous Metabolite
20(S)-Ginsenoside Rg3 (Standard) is the analytical standard of 20(S)-Ginsenoside Rg3. This product is intended for research and analytical applications. 20(S)-Ginsenoside Rg3 is the main component of Panax ginseng C. A. Meyer. Ginsenoside Rg3 inhibits Na+ and hKv1.4 channel with IC50s of 32.2±4.5 and 32.6±2.2 μM, respectively. 20(S)-Ginsenoside Rg3 also inhibits Aβ levels, NF-κB activity, and COX-2 expression.

HY-103332R

N-Arachidonylglycine (Standard) NA-Gly (Standard)	Alkaloids Other Alkaloids Source classification Endogenous metabolite	Reference Standards GlyT Endogenous Metabolite
20(S)-Ginsenoside Rg3 (Standard) is the analytical standard of 20(S)-Ginsenoside Rg3. This product is intended for research and analytical applications. 20(S)-Ginsenoside Rg3 is the main component of Panax ginseng C. A. Meyer. Ginsenoside Rg3 inhibits Na+ and hKv1.4 channel with IC50s of 32.2±4.5 and 32.6±2.2 μM, respectively. 20(S)-Ginsenoside Rg3 also inhibits Aβ levels, NF-κB activity, and COX-2 expression.

Cat. No.	Product Name	Chemical Structure

HY-B1221S1

Flufenamic acid-13C6
Flufenamic acid- ¹³C₆ is the ¹³C₆ labeled Flufenamic acid. Flufenamic acid is a non-steroidal anti-inflammatory agent, inhibits cyclooxygenase (COX), activates AMPK, and also modulates ion channels, blocking chloride channels and L-type Ca ²⁺ channels, modulating non-selective cation channels (NSC), activating K+ channels. Flufenamic acid binds to the central pocket of TEAD2 YBD and inhibits both TEAD function and TEAD-YAP-dependent processes, such as cell migration and proliferation.

Flufenamic acid-13C6

Flufenamic acid- ¹³C₆ is the ¹³C₆ labeled Flufenamic acid. Flufenamic acid is a non-steroidal anti-inflammatory agent, inhibits cyclooxygenase (COX), activates AMPK, and also modulates ion channels, blocking chloride channels and L-type Ca ²⁺ channels, modulating non-selective cation channels (NSC), activating K+ channels. Flufenamic acid binds to the central pocket of TEAD2 YBD and inhibits both TEAD function and TEAD-YAP-dependent processes, such as cell migration and proliferation.

HY-B1221S

Flufenamic acid-d4
Flufenamic acid-d₄ is deuterium labeled Flufenamic acid. Flufenamic acid is a non-steroidal anti-inflammatory agent, inhibits cyclooxygenase (COX), activates AMPK, and also modulates ion channels, blocking chloride channels and L-type Ca ²⁺ channels, modulating non-selective cation channels (NSC), activating K+ channels. Flufenamic acid binds to the central pocket of TEAD2 YBD and inhibits both TEAD function and TEAD-YAP-dependent processes, such as cell migration and proliferation.

Flufenamic acid-d4

Flufenamic acid-d₄ is deuterium labeled Flufenamic acid. Flufenamic acid is a non-steroidal anti-inflammatory agent, inhibits cyclooxygenase (COX), activates AMPK, and also modulates ion channels, blocking chloride channels and L-type Ca ²⁺ channels, modulating non-selective cation channels (NSC), activating K+ channels. Flufenamic acid binds to the central pocket of TEAD2 YBD and inhibits both TEAD function and TEAD-YAP-dependent processes, such as cell migration and proliferation.

HY-132184S

5,6-Epoxyeicosatrienoic acid-d11
5,6-Epoxyeicosatrienoic acid-d₁₁ (5,6-EET-d₁₁) is deuterium labeled 5,6-Epoxyeicosatrienoic acid. 5,6-Epoxyeicosatrienoic acid (5,6-EET; (±)5,6-EpETrE) is a fully racemic version of the enantiomeric forms biosynthesized from arachidonic acid by cytochrome P450 enzymes. In solution, 5,6-Epoxyeicosatrienoic acid degrades into 5,6-DiHET and 5,6-δ-lactone, which can be converted to 5,6-DiHET and quantified by GC-MS. In neuroendocrine cells, such as the anterior pituitary and pancreatic islets, 5,6-Epoxyeicosatrienoic acid has been implicated in the mobilization of calcium and hormone secretion. 5,6-Epoxyeicosatrienoic acid is an inhibitor of T-type voltage-gated calcium channels (Cav3) that inhibits isoforms Cav3.1, Cav3.2 (IC₅₀=0.54 μM), and Cav3. and decreases nifedipine-resistant phenylephrine-induced vasoconstriction in isolated mouse mesenteric arteries via Cav3.2 blockade when used at a concentration of 3 μM. In addition, it is a substrate of COX-1 and COX-2, as measured by oxygen consumption and product formation assays when used at a concentration of 50 μM. (±)5,6-Epoxyeicosatrienoic acid is provided as a mixture of the free acid and lactone .

5,6-Epoxyeicosatrienoic acid-d11

5,6-Epoxyeicosatrienoic acid-d₁₁ (5,6-EET-d₁₁) is deuterium labeled 5,6-Epoxyeicosatrienoic acid. 5,6-Epoxyeicosatrienoic acid (5,6-EET; (±)5,6-EpETrE) is a fully racemic version of the enantiomeric forms biosynthesized from arachidonic acid by cytochrome P450 enzymes. In solution, 5,6-Epoxyeicosatrienoic acid degrades into 5,6-DiHET and 5,6-δ-lactone, which can be converted to 5,6-DiHET and quantified by GC-MS. In neuroendocrine cells, such as the anterior pituitary and pancreatic islets, 5,6-Epoxyeicosatrienoic acid has been implicated in the mobilization of calcium and hormone secretion. 5,6-Epoxyeicosatrienoic acid is an inhibitor of T-type voltage-gated calcium channels (Cav3) that inhibits isoforms Cav3.1, Cav3.2 (IC₅₀=0.54 μM), and Cav3. and decreases nifedipine-resistant phenylephrine-induced vasoconstriction in isolated mouse mesenteric arteries via Cav3.2 blockade when used at a concentration of 3 μM. In addition, it is a substrate of COX-1 and COX-2, as measured by oxygen consumption and product formation assays when used at a concentration of 50 μM. (±)5,6-Epoxyeicosatrienoic acid is provided as a mixture of the free acid and lactone .

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