2. Membrane Transporter/Ion Channel
  3. Na+/H+ Exchanger (NHE)
  4. S3226

S3226 is a highly selective NHE-3 inhibitor (IC50<1 μM) that specifically blocks NHE-3-mediated sodium transport. S3226 significantly inhibits blastocyst formation and expansion in mouse embryos, and reduces fluid and electrolyte reabsorption in rat proximal tubules in a dose-dependent manner. S3226 effectively alleviates ischemia-induced acute renal failure by improving renal function parameters, reducing renal tubular injury and restoring intracellular pH homeostasis, without interfering with the normal tubuloglomerular feedback response. S3226 is widely used in studies of acute renal failure and related pathological mechanisms.

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S3226

S3226 Chemical Structure

CAS No. : 215183-03-2

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S3226 Related Antibodies

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Description

S3226 is a highly selective NHE-3 inhibitor (IC50<1 μM) that specifically blocks NHE-3-mediated sodium transport. S3226 significantly inhibits blastocyst formation and expansion in mouse embryos, and reduces fluid and electrolyte reabsorption in rat proximal tubules in a dose-dependent manner. S3226 effectively alleviates ischemia-induced acute renal failure by improving renal function parameters, reducing renal tubular injury and restoring intracellular pH homeostasis, without interfering with the normal tubuloglomerular feedback response. S3226 is widely used in studies of acute renal failure and related pathological mechanisms[1][2][3].

In Vitro

S3226 acts as a selective inhibitor of NHE3 in transfected mouse fibroblast L cells, opossum kidney cells, and porcine renal brush-border membrane vesicles[2].
S3226 potently inhibits rat NHE3 in fibroblasts transfected with rat NHE3 with an IC50 of 0.2 μM[3].

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

S3226 Related Antibodies
In Vivo

S3226 (4-30 μM; intratubular microperfusion; single application per nephron; 5-minute equilibration before measurement) inhibits proximal convoluted tubule fluid and Na+ reabsorption with an IC50 of 4-5 μM and maximum inhibition of ~30%, but does not affect loop of Henle reabsorption or tubuloglomerular feedback in anesthetized rats[2].
S3226 (20 mg/kg; i.v.; over 30 minutes) improves glomerular filtration rate, renal electrolyte handling, and renal histology, and supports 100% survival in rats with ischemia-induced acute renal failure[3].
S3226 (20 mg/kg; i.v.; over 30 minutes; two doses) significantly reduces renal intracellular pH by 0.15 units during reperfusion in uninephrectomized rats with ischemia-induced acute renal failure[3].

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

Animal Model: Munich-Wistar-Fromter (adult male, 270-350 g, anesthetized with superficial nephrons)[2]
Dosage: 4-5 µM; 10 µM; 30 µM
Administration: intratubular microperfusion; single application per nephron; 5-minute equilibration before measurement
Result: Caused a dose-dependent inhibition of fluid, Na+, and Cl- reabsorption in proximal convoluted tubules with an IC50 of 4-5 µM.
Achieved maximum inhibition of ~30% for fluid and Na+ reabsorption, and ~10% for Cl- reabsorption.
Produced a significantly greater reduction in Na+ reabsorption than in Cl- reabsorption at 10 or 30 µM.
Showed no effect on fluid, Na+, or K+ reabsorption in loop of Henle segments at 10 µM and 30 µM.
Did not alter the tubuloglomerular feedback response, including stop-flow pressure magnitude, curve slope, or operating point shift, at 30 µM.
Animal Model: Wistar (male, mean body weight 285 g, bilateral renal artery occlusion for 40 minutes)[3]
Dosage: 20 mg/kg
Administration: i.v.; over 30 minutes; single dose (pre-occlusion or post-reperfusion)
Result: Increased creatinine clearance to 0.90 mL/min/kg (pre-occlusion treatment) and 0.83 mL/min/kg (post-reperfusion treatment) on day 1 post-ischemia, compared to 0.30 mL/min/kg in controls.
Reduced fractional sodium excretion from 8.17% in controls to 1.42% (pre-occlusion treatment) and 1.88% (post-reperfusion treatment) on day 1.
Reduced urinary sodium excretion to 0.31 mmol/kg (pre-occlusion treatment) and 0.31 mmol/kg (post-reperfusion treatment) on day 1, compared to 0.98 mmol/kg in controls.
Lowered plasma creatinine elevation on days 1, 2, and 3 post-infusion compared to controls.
Lowered plasma potassium concentration on days 2 and 3 compared to controls.
Reduced fractional potassium excretion on day 1 compared to controls.
Pronounced reduction of tubular necrosis, dilatation, protein casts, and cellular infiltration in kidneys harvested on day 7.
Achieved 100% survival rate over 7 days, compared to 75% survival rate in controls.
Molecular Weight

415.32

Formula

C17H24Cl2N6O2
CAS No.
Appearance

Solid

Color

White to off-white

SMILES

[H]Cl.[H]Cl.C/C(C(NC(N)=N)=O)=C\C(C=CC(C)=C1)=C1/C=C(C)/C(NC(N)=N)=O
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

4°C, stored under nitrogen, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen, away from moisture)

Purity & Documentation
References
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S3226 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

S3226215183-03-2S 3226S-3226Na+/H+ Exchanger (NHE)Sodium/hydrogen ExchangerSodium-hydrogen ExchangerNa+/H+ exchanger-3ratloop of HenleNHE-3ischemia-induced acute renal failureproximal convoluted tubuletubuloglomerular feedbacktransfected fibroblastsblastocystmouse embryoInhibitorinhibitorinhibit

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