NKCC Inhibitor

Sodium dichloroacetate is an orally active pyruvate dehydrogenase kinase (PDK) inhibitor. Sodium dichloroacetate also stimulates pyruvate dehydrogenase (PDH) activity and works as a Na⁺-K⁺-2Cl⁻ cotransporter (NKCC) inhibitor. Sodium dichloroacetate prevents the phosphorylation of the E1α subunit of PDC, promoting the entry of pyruvate into the mitochondria for oxidative metabolism, reducing lactate production, and simultaneously increasing the production of reactive oxygen species (ROS). Sodium dichloroacetate inhibits tumor cell proliferation and induces apoptosis. Sodium dichloroacetate is promising for research of cancers.

Bumetanide (Ro 10-6338; PF 1593), a highly potent loop diuretic, is a Na⁺-K⁺-Cl⁺ cotransporter (NKCC) blocker. Bumetanide is a selective NKCC1 inhibitor, but also inhibits NKCC2, with IC₅₀s of 0.68 μM and 4.0 μM for hNKCC1A and hNKCC2A, respectively.

Furosemide is an orally active NKCC2 inhibitor that can cross the blood-brain barrier. Furosemide inhibits NKCC1, NKCC2, KCC2, KCC3, and KCC4. Furosemide selectively antagonizes GABA_A receptors containing α6 and β2/3 or β3γ2 subunits. Furosemide penetrates the blood-brain barrier and blocks renal tubular sodium-chloride reabsorption, increases urinary excretion of sodium, chloride, potassium, and calcium, and activates the renin-angiotensin-aldosterone system. Furosemide can be used in research on congestive heart failure, hypertension, and edema.

ZT-1a is a potent, non-ATP-competitive and selective SPAK inhibitor. ZT-1a inhibits SPAK activity with IC₅₀s of 44.3, 35.0, 46.7 μM at ATP concentrations of 0.01, 0.1 and 1 mM, respectively.

Azosemide, a sulfonamide loop diuretic, is a potent NKCC1 inhibitor with IC₅₀s of 0.246 μM and 0.197 μM for hNKCC1A and NKCC1B, respectively.

Furosemide sodium is an orally active NKCC2 inhibitor that can cross the blood-brain barrier. Furosemide sodium inhibits NKCC1, NKCC2, KCC2, KCC3, and KCC4. Furosemide sodium selectively antagonizes GABA_A receptors containing α6 and β2/3 or β3γ2 subunits. Furosemide sodium penetrates the blood-brain barrier and blocks renal tubular sodium-chloride reabsorption, increases urinary excretion of sodium, chloride, potassium, and calcium, and activates the renin-angiotensin-aldosterone system. Furosemide sodium can be used in research on congestive heart failure, hypertension, and edema.

IAMA-6 is a selective NKCC1 inhibitor with neuroprotective effects. IAMA-6 can be used for the study of brain conditions, including drug-resistant epilepsy (e.g. temporal lobe epilepsy (TLE) and Dravet syndrome (DrS)), autism spectrum disorders (ASD) and Down syndrome (DoS).

Bendroflumethiazide (Bendrofluazide) is an orally available diuretic. Bendroflumethiazide inhibits the electroneutral sodium-chloride symporter located in the apical membrane of the early segment of the distal convoluted tubule and can effectively lower blood pressure. Bendroflumethiazide is used in the study of hypertension and edema. Bendroflumethiazide has an antidiuretic effect in diabetes insipidus.

Torsemide (Torasemide) is an orally active loop diuretic. Torsemide has anti-aldosterone and vasodilatory effects. Torsemide also can be used for the research of heart failure, renal disease and hepatic cirrhosis.

Furosemide (Standard) is the analytical standard of Furosemide (HY-B0135). This product is intended for research and analytical applications. Furosemide is an orally active NKCC2 inhibitor that can cross the blood-brain barrier. Furosemide inhibits NKCC1, NKCC2, KCC2, KCC3, and KCC4. Furosemide selectively antagonizes GABA_A receptors containing α6 and β2/3 or β3γ2 subunits. Furosemide penetrates the blood-brain barrier and blocks renal tubular sodium-chloride reabsorption, increases urinary excretion of sodium, chloride, potassium, and calcium, and activates the renin-angiotensin-aldosterone system. Furosemide can be used in research on congestive heart failure, hypertension, and edema.

Torsemide (Standard) is the analytical standard of Torsemide. This product is intended for research and analytical applications. Torsemide (Torasemide) is an orally active loop diuretic. Torsemide has anti-aldosterone and vasodilatory effects. Torsemide also can be used for the research of heart failure, renal disease and hepatic cirrhosis.

Furosemide-d₅ is the deuterated-labeled Furosemide (HY-B0135). Furosemide is an orally active NKCC2 inhibitor that can cross the blood-brain barrier. Furosemide inhibits NKCC1, NKCC2, KCC2, KCC3, and KCC4. Furosemide selectively antagonizes GABA_A receptors containing α6 and β2/3 or β3γ2 subunits. Furosemide penetrates the blood-brain barrier and blocks renal tubular sodium-chloride reabsorption, increases urinary excretion of sodium, chloride, potassium, and calcium, and activates the renin-angiotensin-aldosterone system. Furosemide can be used in research on congestive heart failure, hypertension, and edema.

Bendroflumethiazide-d₅ (Bendrofluazide-d₅) is the deuterium labeled Bendroflumethiazide (HY-B1363).Bendroflumethiazide (Bendrofluazide) is an orally available diuretic. Bendroflumethiazide inhibits the electroneutral sodium-chloride symporter located in the apical membrane of the early segment of the distal convoluted tubule and can effectively lower blood pressure. Bendroflumethiazide is used in the study of hypertension and edema. Bendroflumethiazide has an antidiuretic effect in diabetes insipidus.

Bumetanide (Standard) is the analytical standard of Bumetanide. This product is intended for research and analytical applications. Bumetanide (Ro 10-6338; PF 1593), a highly potent loop diuretic, is a Na⁺-K⁺-Cl⁺ cotransporter (NKCC) blocker. Bumetanide is a selective NKCC1 inhibitor, but also inhibits NKCC2, with IC₅₀s of 0.68 μM and 4.0 μM for hNKCC1A and hNKCC2A, respectively.

Bumetanide-d₅ is a deuterium labeled Bumetanide. Bumetanide is a selective Na+-K+-Cl- (NKCC1) inhibitor, weakly inhibits NKCC2, with ?IC₅₀s of 0.68 and 4.0 μM for hNKCC1A and hNKCC2A, respectively.

Bendroflumethiazide (Standard) (Bendrofluazide (Standard)) is the analytical standard of Bendroflumethiazide (HY-B1363). This product is intended for research and analytical applications. Bendroflumethiazide (Bendrofluazide) is an orally available diuretic. Bendroflumethiazide inhibits the electroneutral sodium-chloride symporter located in the apical membrane of the early segment of the distal convoluted tubule and can effectively lower blood pressure. Bendroflumethiazide is used in the study of hypertension and edema. Bendroflumethiazide has an antidiuretic effect in diabetes insipidus.

Furosemide (sodium) (Standard) is the analytical standard of Furosemide (sodium). This product is intended for research and analytical applications. Furosemide sodium is a potent and orally active inhibitor of Na+/K+/2Cl- (NKCC) cotransporter, NKCC1 and NKCC2. Furosemide sodium is also a GABAA receptors antagonist and displays 100-fold selectivity for α6-containing receptors than α1-containing receptors. Furosemide sodium acts as a loop diuretic and used for the study of congestive heart failure, hypertension and edema.

Bumetanide solution is mainly composed of Bumetanide (HY-17468). Bumetanide (Ro 10-6338; PF 1593), a highly potent loop diuretic, is a Na⁺-K⁺-Cl⁺ cotransporter (NKCC) blocker. Bumetanide is a selective NKCC1 inhibitor, but also inhibits NKCC2, with IC₅₀s of 0.68 μM and 4.0 μM for hNKCC1A and hNKCC2A, respectively.

Bumetanide sodium, a highly potent loop diuretic, is a Na⁺-K⁺-Cl⁺ cotransporter (NKCC) blocker. Bumetanide sodium is a selective NKCC1 inhibitor, and also inhibits NKCC2, with IC₅₀s of 0.68 and 4.0 μM for hNKCC1A and hNKCC2A, respectively.

Triflocin is an orally active diuretic and Na⁺-K⁺-2Cl⁻ cotransporter inhibitor with an IC₅₀ of 3×10^-5 M. Triflocin inhibits the outward basolateral electrogenic Na-(HCO3) n>1 cotransport in the proximal tubule. Triflocin has no tendency to induce hyperglycemia, and its blood glucose-elevating effect is extremely weak, such that an increase in blood glucose levels can only be detected under special conditions such as glucose loading. Triflocin is more prone to induce hypoglycemia.