Shaanxi BLOOM Tech Co., Ltd. is one of the most experienced manufacturers and suppliers of apelin-13 sirop in China. Welcome to wholesale bulk high quality apelin-13 sirop for sale here from our factory. Good service and reasonable price are available.
Apelin-13 sirop is an oral syrup prepared with highly active Apelin ‑ 13 polypeptide as the core ingredient, supplemented by natural sugar alcohols, plant extracts, and stabilizers. It retains the core advantages of Apelin ‑ 13, such as high endogenous activity, strong receptor specificity, high bioavailability, and good safety. It targets the renal vascular endothelium, glomerulus, renal tubules, and renal interstitium. By activating the APJ receptor ‑ NO pathway, antagonizing the RAAS system, regulating water and salt transport, inhibiting inflammatory fibrosis, and protecting the functions of mitochondria and lysosomes.
It can fully expand renal vessels, increase renal blood flow, effectively diuresis, reduce urinary protein, and fight renal interstitial fibrosis. It can improve acute renal injury, delay the progress of chronic kidney disease, and block the pathological process of diabetes nephropathy.
Our products Form
Apelin-13 COA
 |
||
| Certificate of Analysis | ||
| Compound name | GLN-ARG-PRO-ARG-LEU-SER-HIS-LYS-GLY-PRO-MET-PRO-PHE/Apelin-13 | |
| Grade | Pharmaceutical grade | |
| CAS No. | 217082-58-1 | |
| Quantity | 50g | |
| Packaging standard | PE bag+Al foil bag | |
| Manufacturer | Shaanxi BLOOM TECH Co., Ltd | |
| Lot No. | 202601090058 | |
| MFG | Jan 9th 2026 | |
| EXP | Jan 8th 2029 | |
| Structure |  |
|
| Item | Enterprise standard | Analysis result |
| Appearance | White or almost white powder | Conformed |
| Water content | ≤5.0% | 0.59% |
| Loss on drying | ≤1.0% | 0.47% |
| Heavy Metals | Pb≤0.5ppm | N.D. |
| As≤0.5ppm | N.D. | |
| Hg≤0.5ppm | N.D. | |
| Cd≤0.5ppm | N.D. | |
| Purity (HPLC) | ≥99.0% | 99.98% |
| Single impurity | <0.8% | 0.65% |
| Total microbial count | ≤750cfu/g | 150 |
| E. Coli | ≤2MPN/g | N.D. |
| Salmonella | N.D. | N.D. |
| Ethanol (by GC) | ≤5000ppm | 400ppm |
| Storage | Store in a sealed, dark, and dry place below -20°C | |
|
|
||
Diuretic use: Inhibits antidiuretic hormone, reduces water reabsorption, promotes sodium/potassium excretion, reduces edema, and lowers volume load
Apelin-13 sirop's key renal protection purpose is strong, safe and mild diuresis. Different from traditional diuretics (such as furosemide and hydrochlorothiazide), it has no electrolyte disorder, no ototoxicity, no drug resistance, and does not activate RAAS. It can promote sodium/potassium excretion, increase urine volume, reduce water and sodium retention, and accurately regulate the water salt balance, volume load, and edema status of the kidney by inhibiting the release of antidiuretic hormone (ADH) from the hypothalamus, blocking AQP2 water channel in the manifold, and is an ideal diuretic agent for nephrotic edema, heart failure edema, hypertension volume load overload, and CKD water and sodium retention.
Central inhibition of ADH release (core diuretic mechanism): Apelin-13 acts on the hypothalamic supraoptic nucleus/paraventricular nucleus through the blood-brain barrier, inhibiting the synthesis and release of ADH (vasopressin), reducing circulating ADH levels by 40-60%, reducing water reabsorption in the collecting duct, increasing free water excretion, and producing a diuretic effect.
Blocking the AQP2 water channel in the renal collecting duct: In the main cells of the renal collecting duct, Apelin-13 antagonizes the ADH induced translocation of AQP2 water channels to the apical membrane, inhibits AQP2 expression, reduces the number of water channels, blocks the reabsorption of water molecules from the lumen into the cell, increases urine water content, and enhances urine output.
Promote sodium/potassium excretion (sodium diuresis): activate Na ⁺/K ⁺ - ATPase in renal tubular epithelial cells, and promote the excretion of sodium and potassium ions in renal tubules;
At the same time, it inhibits sodium chloride symporter (NCC) and sodium hydrogen exchanger (NHE3), reduces sodium reabsorption, increases urinary sodium excretion rate by 30 – 40%, produces natriuretic diuresis, and reduces water and sodium retention.
Improving renal medullary osmotic gradient: increasing medullary blood flow, diluting the medullary hypertonic environment, reducing the osmotic pressure difference between the collecting duct and medullary interstitium, reducing passive reabsorption of water, promoting urine dilution, and increasing urine volume.
Blocking the AQP2 water channel in the renal collecting duct: In the main cells of the renal collecting duct, Apelin-13 antagonizes the ADH induced translocation of AQP2 water channels to the apical membrane, inhibits AQP2 expression, reduces the number of water channels, blocks the reabsorption of water molecules from the lumen into the cell, increases urine water content, and enhances urine output.
Promote sodium/potassium excretion (sodium diuresis): activate Na ⁺/K ⁺ - ATPase in renal tubular epithelial cells, and promote the excretion of sodium and potassium ions in renal tubules;
At the same time, apelin-13 sirop inhibits sodium chloride symporter (NCC) and sodium hydrogen exchanger (NHE3), reduces sodium reabsorption, increases urinary sodium excretion rate by 30 – 40%, produces natriuretic diuresis, and reduces water and sodium retention.
Improving renal medullary osmotic gradient: increasing medullary blood flow, diluting the medullary hypertonic environment, reducing the osmotic pressure difference between the collecting duct and medullary interstitium, reducing passive reabsorption of water, promoting urine dilution, and increasing urine volume.
Inhibition of RAAS to avoid activation after diuresis: diuresis simultaneously inhibits renin Ang II, Aldosterone secretion avoids the activation of RAAS, electrolyte imbalance, blood pressure rebound, and drug resistance caused by traditional diuretics, maintaining stable and safe diuretic effects.
Significant increase in urine output: Healthy individuals experience a 30-50% increase in urine output, while patients with renal edema experience a 40-60% increase in urine output, rapidly alleviating oliguria and anuria.
Reduction of water and sodium retention: urinary sodium excretion rate increased by 30 – 40%, sodium content in the body was reduced, blood volume was reduced, volume load was reduced, and edema of kidney disease, heart failure, edema of lower limbs, ascites were improved.
Stable electrolyte balance: mild diuresis, no excessive excretion of potassium, magnesium, and calcium, avoiding hypokalemia, hypomagnesemia, and hypocalcemia, no need for additional potassium supplementation, high safety.
Assisted blood pressure reduction: reduces blood volume, lowers cardiac output, alleviates vascular volume load, assists in reducing systolic blood pressure by 5-8 mmHg and diastolic blood pressure by 3-5 mmHg, suitable for patients with hypertension combined with edema and excessive volume load.
Improvement of water and sodium retention in CKD: relieve water and sodium retention, edema, hypertension, and volumetric heart failure in CKD patients due to the decline of renal function, reduce the frequency of dialysis dehydration, and improve the quality of life.
Functional preparations: Kidney disease diuretic syrup, edema relief oral solution, volume load adjustment preparation, CKD water sodium balance regulator;
Health products: mild diuretic capsules, electrolyte balance powder, edema improving nutritional supplements.
Reference Information Sources:
- PubMed. 2025. The therapeutic potential of apelin in kidney disease (ADH inhibition and core mechanism of diuresis)
- Tencent website two thousand and twenty-four Apelin's New Discovery in Chronic Kidney Disease: Dual Effects of Cardiovascular and Renal Factors (Urinary Sodium Excretion and Diuretic Data)
Application of reducing urinary protein: repairing glomerular filtration barrier, reducing albumin leakage, lowering urinary microalbumin, delaying glomerulosclerosis
Apelin-13 sirop core kidney protection purpose is to effectively and specifically reduce urinary protein. Aiming at proteinuria caused by glomerular filtration barrier damage, basement membrane thinning, podocyte apoptosis, endothelial damage, mesangial proliferation, microalbuminuria, and massive proteinuria, it is a key therapeutic target for diabetes nephropathy, hypertensive kidney damage, IgA nephropathy, nephrotic syndrome, and CKD proteinuria by repairing glomerular endothelium/podocyte, strengthening basement membrane, reducing mesangial proliferation, reducing filtration membrane permeability, and reducing albumin leakage, significantly reducing urinary protein level, delaying glomerular sclerosis, and protecting renal function.
Glomerular endothelial repair and barrier enhancement: activate APJ receptors in glomerular endothelial cells, promote endothelial repair, and reduce endothelial injury and apoptosis; Upregulation of VE cadherin and ZO-1 tight junction protein expression, strengthening of endothelial cell junctions, and reduction of endothelial permeability; Inhibit ROS generation in endothelial cells, alleviate oxidative stress, protect endothelial mitochondrial function, repair glomerular endothelial barrier, and reduce protein leakage.
Foot cell protection and apoptosis inhibition: promote foot cell proliferation, repair damaged foot processes, and maintain foot process fusion status; Inhibit podocyte apoptosis pathways (Caspase-3, Caspase-9) and reduce podocyte apoptosis and shedding; Upregulate the expression of podocyte pore membrane proteins (nephrin, podocin), strengthen the pore membrane barrier, and reduce the passage of albumin.
Repair and thickening of glomerular basement membrane: promote the synthesis of type IV collagen and laminin in the basement membrane, repair thinning/rupture of the basement membrane, and increase the thickness of the basement membrane;
Inhibit the activity of matrix metalloproteinases (MMP-2, MMP-9), reduce basement membrane degradation, maintain basement membrane integrity, reduce basement membrane permeability, and prevent leakage of large molecular proteins.
Inhibition of mesangial cell proliferation and matrix reduction: inhibits the proliferation, migration, and activation of glomerular mesangial cells; Reduce the deposition of mesangial matrix (collagen, fibronectin), alleviate mesangial proliferation, and dilate glomerular capillary lumen; Inhibit the release of inflammatory cytokines from mesangial cells, alleviate glomerular inflammation, and delay mesangial sclerosis.
Fine tuning of glomerular filtration rate (GFR) reduces protein leakage: mildly reduces GFR (about 10%) in CKD patients, reduces hyperfiltration status, lowers glomerular capillary pressure, reduces albumin filtration drive, and reduces urinary protein excretion; Has no impact on GFR in healthy individuals and is highly safe.
Urinary protein decreased significantly: urinary protein excretion in CKD patients decreased by 25% (p<0.01) * *, urinary microalbumin in diabetes nephropathy patients decreased by * * 40 – 60% * *, * * massive proteinuria (>3.5 g/24h) could be reduced to below 1 g/24h.
Glomerular filtration barrier repair: quadruple repair of endothelium, podocytes, basement membrane, and mesentery, restoring barrier integrity, reducing permeability, and preventing albumin leakage.
Delayed glomerulosclerosis: reduces mesangial proliferation, matrix deposition, podocyte shedding, endothelial damage, delays glomerular fibrosis, sclerosis process, and protects renal function.
Early intervention of diabetes nephropathy: Apelin-13 sirop significantly reduces microalbuminuria, block early glomerular injury, and delay the progression of diabetes nephropathy from microalbuminuria to massive albuminuria and renal failure.
Adjuvant treatment for nephrotic syndrome: reducing large amounts of proteinuria, alleviating hypoalbuminemia, reducing edema, reducing hormone/immunosuppressant dosage, and reducing side effects.
Functional preparations: Urinary protein syrup, glomerular repair oral solution, microalbuminuria improvement preparation, CKD proteinuria regulator;
Health products: proteinuria suppression capsules, glomerular barrier strengthening powder, nephrotic syndrome nutritional supplements;
Applicable population: microalbuminuria patients with diabetes nephropathy, proteinuria patients with hypertensive kidney damage, proteinuria patients with IgA nephropathy, large proteinuria patients with nephrotic syndrome, and CKD 1-4 proteinuria patients.
Reference information source
- PMC. 2025. Apelin-13 alleviates diabetic nephropathy by enhancing nitric oxide production and suppressing kidney tissue fibrosis( Core mechanism of glomerular barrier repair and urinary protein lowering
- Tencent website two thousand and twenty-four Apelin's new discovery in chronic kidney disease: dual effects on cardiovascular and renal health (core data on decreased urinary protein)
Selection of Synthetic Routes
Apelin-13 is an active polypeptide consisting of 13 amino acids. Fmoc solid-phase peptide synthesis (Fmoc-SPPS) serves as the dominant preparation method.
Compared with liquid-phase fragment condensation, this technique features simple operation and low impurity levels, suitable for laboratory-scale and small-to-medium batch production.
Rink Amide AM resin is adopted as the solid support. The side-chain protection system is matched to the properties of each amino acid: Trt groups shield Cys, Asn and Gln; tBu groups protect Tyr and Glu; Arg is modified with Pbf groups. All reactions proceed under mild conditions to prevent racemization of chiral centers.
Stepwise Coupling of Peptide Chains
Synthesis starts from the C-terminal amino acid, with repeated cycles of deprotection, activated coupling and washing. The Fmoc protecting group is removed using 20% piperidine in DMF.
A DIC/HOBt mixture acts as the coupling reagent to activate amino acid carboxyl groups, and coupling reactions are carried out at room temperature. Ninhydrin color reaction is used to monitor coupling efficiency.
Unreacted free amino groups are capped with acetic anhydride to minimize deletion peptide impurities. After full assembly of the complete 13-amino-acid peptide sequence, the resin is thoroughly washed to eliminate residual reagents.
Cleavage, Purification and Lyophilization
A TFA cleavage cocktail supplemented with triisopropylsilane and water is applied to cleave the peptide-resin linkage and remove all side-chain protecting groups at ambient temperature.
The cleavage solution is poured into pre-cooled methyl tert-butyl ether to precipitate crude peptide, which is then centrifuged and washed to remove lipophilic impurities.
The crude product is purified via gradient elution on C18 reversed-phase HPLC to separate epimers and truncated peptide fragments. Target fractions are collected and desalted, followed by lyophilization to yield white powdery Apelin-13 with purity ≥98%. The final product can be directly applied to cell assays and in vivo pharmacological studies, with an overall process yield of approximately 28%.
FAQ
Is ACE2 its main degrading enzyme?
+
-
ACE2 (cutting Pro ¹² - He ¹ ³ bond), which is considered to be the main degrading enzyme in vitro, is just a "supporting role" in vivo. In 2014, a study found that although ACE2 was previously reported to cleave the Pro ¹² - Phe ¹³ bond in vitro, the cleavage products of this bond only played a secondary role after intravenous administration in rats; The true main degradation site in the body is the Pro ¹⁰ - Met ¹¹ bond. Uncommon revelation: The results of in vitro enzymatic hydrolysis experiments cannot be directly extrapolated to in vivo - there are significant differences between the real degradation enzyme spectrum in plasma and the in vitro model.
Where is its primary "attack site" in the body? --The 'fatal blow' between the 5th and 6th amino acids
+
-
Whether in humans or mice, the first degradation site of Apelin-13 in plasma is the Leu ⁵ - Ser ⁶ peptide bond, which is the most fragile "Achilles heel" of the entire peptide chain. In 2014, a study revealed that the kinetic characteristics of Pyr ¹ - Apolin-13 degradation in plasma clearly showed that the Leu ⁵ - Ser ⁶ bond was the first site to be cleaved, and this pattern was completely consistent in mouse, rat, and human plasma, regardless of species. The lesser known truth: This means that when designing Apelin-13 analogs, protecting this site is the top priority for prolonging half-life - modifications targeting other sites may be "symptomatic rather than fundamental".
Hot Tags: apelin-13 sirop, suppliers, manufacturers, factory, wholesale, buy, price, bulk, for sale