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Sodium phosphate dibasic, meets analytical specification of Ph. Eur. BP USP FCC E339  (Synonyms: Disodium hydrogen phosphate, meets analytical specification of Ph. Eur. BP USP FCC E339)

Cat. No.: HY-Y0308D
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Sodium phosphate dibasic (Disodium hydrogen phosphate), meets analytical specification of Ph. Eur. BP USP FCC E339 is an inorganic dibasic phosphate that functions as an electrolyte supplement, a buffer carrier for injectable drugs, while also exhibiting nephrotoxicity. Sodium phosphate dibasic, meets analytical specification of Ph. Eur. BP USP FCC E339 induces extensive nephrotic syndrome-like changes, including systemic symptoms such as persistent proteinuria, lipemia, hypercholesterolemia, and anemia, and causes severe renal pathological alterations such as renal enlargement, glomerular calcification, podocyte injury, and tubulointerstitial lesions. Sodium phosphate dibasic, meets analytical specification of Ph. Eur. BP USP FCC E339 has the ability to induce phosphate-induced nephropathy and glomerular calcification, and can be widely used in studies on nephrotic syndrome and related renal pathological mechanisms.

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Sodium phosphate dibasic, meets analytical specification of Ph. Eur. BP USP FCC E339

Sodium phosphate dibasic, meets analytical specification of Ph. Eur. BP USP FCC E339 Chemical Structure

CAS No. : 7558-79-4

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Description

Sodium phosphate dibasic (Disodium hydrogen phosphate), meets analytical specification of Ph. Eur. BP USP FCC E339 is an inorganic dibasic phosphate that functions as an electrolyte supplement, a buffer carrier for injectable drugs, while also exhibiting nephrotoxicity. Sodium phosphate dibasic, meets analytical specification of Ph. Eur. BP USP FCC E339 induces extensive nephrotic syndrome-like changes, including systemic symptoms such as persistent proteinuria, lipemia, hypercholesterolemia, and anemia, and causes severe renal pathological alterations such as renal enlargement, glomerular calcification, podocyte injury, and tubulointerstitial lesions. Sodium phosphate dibasic, meets analytical specification of Ph. Eur. BP USP FCC E339 has the ability to induce phosphate-induced nephropathy and glomerular calcification, and can be widely used in studies on nephrotic syndrome and related renal pathological mechanisms[1][2][3].

In Vivo

Sodium phosphate dibasic, meets analytical specification of Ph. Eur. BP USP FCC E339 (409.6 mg/kg/day; tail vein; once daily; 14 or 28 days) induces irreversible, progressive nephrotic syndrome in male Sprague-Dawley rats, characterized by persistent proteinuria, a 60% reduction in albumin/globulin ratio, up to 6.4-fold elevated cholesterol, up to 4.8-fold elevated triglycerides, up to 1.4-fold elevated platelets, up to 2.3-fold elevated fibrinogen, a slight decrease in serum Ca2+ only in the 28-day group, and severe renal morphological damage that worsens during withdrawal[1].
Sodium phosphate dibasic, meets analytical specification of Ph. Eur. BP USP FCC E339 (360 mM (409.6 mg/kg/day); i.v.; once daily; single dose, 3 consecutive days, or 8 consecutive days) induces progressive glomerular damage including proteinuria, podocyte injury, and calcification in male Sprague-Dawley rats, with all treated rats showing moderate to severe proteinuria by day 8 and glomerular calcification evident after 8 days of dosing[2].
Sodium phosphate dibasic (1-408 mg/kg; i.v.; once daily; 14 days) induces dose-dependent glomerular calcification, epithelial degeneration, and proteinuria in male Sprague-Dawley rats at 284 mg/kg and 408 mg/kg, with no adverse effects observed at 1 mg/kg or 28 mg/kg[3].

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

Animal Model: Jcl:SD (male, 5 weeks old at study start, nephrotic syndrome induced by daily tail-vein injections of dibasic sodium phosphate)[1]
Dosage: 360 mM (409.6 mg/kg/day) (14-day treatment + 14-day withdrawal; 28-day treatment)
Administration: tail vein; once daily; 14 days followed by 14-day withdrawal; once daily; 28 days
Result: Detected persistent proteinuria first on day 3, with all treated rats showing moderate to severe proteinuria from day 8 onward; proteinuria persisted without remission after the 14-day withdrawal period.
Increased total cholesterol up to 6.4-fold in the 28-day group and 5.3-fold in the withdrawal group.
Increased triglycerides up to 4.8-fold in the 28-day group.
Reduced albumin/globulin ratio by 60% in the 28-day group and 57% in the withdrawal group.
Decreased red blood cell count, hematocrit, and hemoglobin levels to 70-80% of control values.
Increased platelet count up to 1.4-fold.
Increased fibrinogen levels up to 2.3-fold.
Kept serum inorganic phosphorus levels unchanged relative to controls.
Caused a slight decrease in serum calcium only in the 28-day group, with no change in the withdrawal group.
Increased absolute kidney weight to 1.71-fold of control in the 28-day group and 1.31-fold of control in the withdrawal group; kidneys appeared pale, markedly enlarged, and had a rough surface.
Induced glomerular lesions including widespread mineralization, capillary dilatation, partial adhesion of glomerular tufts to Bowman’s capsule, mesangiolysis, and occasional mesangial sclerosis.
Induced tubulointerstitial lesions including tubular regeneration, dilatation, protein casts, basement membrane mineralization, focal interstitial inflammation, and fibrosis; lesions worsened during the withdrawal period despite no further treatment.
Revealed glomerular basement membrane thickening, podocyte foot process effacement, increased podocyte microvilli, and lamellar structure deposits in glomerular tissues via electron microscopy.
Showed significant reduction in podoplanin-positive podocytes and increased desmin expression in podocytes of treated rats via immunohistochemistry.
Observed spleen enlargement and extramedullary hematopoiesis in the 28-day group.
Detected focal mineralization in lung alveolar septa, heart small artery walls, aortic arch endothelium, and thyroid/parathyroid interstitium in the 28-day group, and in thyroid glands in the withdrawal group.
Animal Model: Jcl:SD (male, 6 weeks of age)[2]
Dosage: 360 mM (409.6 mg/kg/day)
Administration: i.v.; once daily; single dose, 3 consecutive days, or 8 consecutive days
Result: Detected no increased urinary protein after single dosing.
Observed increased urinary protein (100 mg/dl/4 hr, 2+) in 2/10 treated rats on day 3.
Found almost all treated rats had urinary protein levels of 100-1000 mg/dl/4 hr (2+ to 4+) on day 5.
Showed all treated rats had moderate to severe proteinuria by day 8.
Detected no glomerular lesions after single dosing.
Observed minimal/focal calcium deposition in parietal epithelial cells in 2/5 rats after 3 days of dosing.
Identified focal calcification of glomerular basement membrane (GBM) and mesangium, plus minimal to mild calcium deposition in parietal epithelial cells, accompanied by hypertrophy and increased mitotic figures in parietal epithelial cells after 8 days of dosing.
Observed small vacuoles scattered in Bowman’s space, small vacuoles in podocyte cytoplasm, and partially electron-dense, irregularly thickened capillary endothelium after single dosing.
Found low-density lamellar structures in Bowman’s space, GBM, and mesangial matrix, podocyte hypertrophy, podocyte foot process effacement, increased microvilli, and debris-filled Bowman’s space after 3 days of dosing.
Detected severe podocyte degeneration, accreted lamellar structures in parietal epithelia, podocytes, and GBM, and thickened GBM after 8 days of dosing.
Observed increased desmin expression in glomerular tufts, decreased podoplanin expression in podocytes and parietal epithelial cells, and a tendency toward increased numbers of PCNA-positive podocytes and parietal epithelial cells on day 9.
Molecular Weight

141.96

Formula

Na2HPO4

CAS No.
SMILES

[Na2HPO4]

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Sodium phosphate dibasic, meets analytical specification of Ph. Eur. BP USP FCC E339
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HY-Y0308D
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