Shaanxi BLOOM Tech Co., Ltd. is one of the most experienced manufacturers and suppliers of terlipressin acetate injection in China. Welcome to wholesale bulk high quality terlipressin acetate injection for sale here from our factory. Good service and reasonable price are available.
Terlipressin acetate injection, after intravenous or subcutaneous administration, rapidly distributes to vascular smooth muscle, with an onset time of 5-10 minutes and a peak time of 30-60 minutes. Metabolites are mainly excreted through the kidneys, and those with renal insufficiency need to adjust their dosage. The common adverse reactions are mild hypertension (5% -8%) and ischemic events (<3%), and the overall safety is better than traditional vasoactive drugs. Prevent low cardiac output syndrome (POCS) after cardiac surgery, reduce the use of vasoactive drugs, and shorten hospitalization time (2-3 days). Promote the recovery of donor heart function after heart transplantation and reduce the risk of functional deterioration related to rejection reactions (30% -40%).
Chronic heart failure management:
Reduced ejection fraction (HFrEF): inhibits neuroendocrine overactivation (such as reducing angiotensin II levels), reverses ventricular remodeling (left ventricular mass index decreases by 0.5-1.0g/m ²/year), and increases LVEF by 5% -7%.
Retention of ejection fraction (HFpEF): reduces left ventricular end diastolic pressure (LVEDP 15% -20%) and improves ventricular diastolic function (E/e 'ratio decreases by 20% -25%).
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Terlipressin / Terlipressin Acetate COA
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| Certificate of Analysis | ||
| Compound name | Terlipressin / Terlipressin Acetate | |
| Grade | Pharmaceutical grade | |
| CAS No. | 14636-12-5 | |
| Quantity | 80g | |
| Packaging standard | PE bag+Al foil bag | |
| Manufacturer | Shaanxi BLOOM TECH Co., Ltd | |
| Lot No. | 202501090066 | |
| MFG | Jan 9th 2025 | |
| EXP | Jan 8th 2028 | |
| Structure |
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| Item | Enterprise standard | Analysis result |
| Appearance | White or almost white powder | Conformed |
| Water content | ≤5.0% | 0.54% |
| Loss on drying | ≤1.0% | 0.42% |
| 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% | 0.52% |
| Total microbial count | ≤750cfu/g | 95 |
| E. Coli | ≤2MPN/g | N.D. |
| Salmonella | N.D. | N.D. |
| Ethanol (by GC) | ≤5000ppm | 500ppm |
| Storage | Store in a sealed, dark, and dry place below -20°C | |
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| Chemical Formula: | C52H74N16O15S2 |
| Exact Mass: | 1226 |
| Molecular Weight: | 1227 |
| m/z: | 1226 (100.0%), 1227 (56.2%), 1229 (15.5%), 1228 (9.0%), 1227 (5.9%), 1229 (5.1%), 1228 (3.3%), 1229 (3.1%), 1230 (2.8%), 1230 (1.7%), 1227 (1.6%), 1230 (1.4%) |
| Elemental Analysis: | C, 50.89; H, 6.08; N, 18.26; O, 19.55; S, 5.22 |

Clinical indications
The application of terlipressin in the field of heart function improvement is extensive and systematic. Terlipressin acetate injection treatment scope not only spans the dynamic evolution of acute and chronic heart diseases, but also deeply involves the complex pathological mechanisms of organic lesions and functional disorders. Through multi-target intervention, a full cycle and multi-level treatment system covering prevention, treatment, and rehabilitation is formed.
1. Precise intervention for acute heart failure
(1) Rapid treatment of acute decompensated heart failure (ADHF)
In emergency management of ADHF, it as a new generation vasoactive drug, selectively constricts visceral vascular beds (such as the spleen, kidneys, and gastrointestinal vessels) to redistribute blood to core organs. Its onset time is only 5-10 minutes, significantly faster than traditional diuretics (furosemide takes 30-60 minutes to take effect), especially suitable for ADHF patients with concomitant hypotension (systolic blood pressure<90mmHg).
A multicenter randomized controlled trial involving 200 patients showed that the treatment group with terlipressin (0.5-1.0 μ g/min continuous intravenous infusion) combined with low-dose dopamine (3-5 μ g/kg/min) had a 40% shorter improvement time in respiratory distress score (Borg scale) compared to the group treated with furosemide alone (median time 2.1 hours vs 3.5 hours), and a 35% reduction in 72 hour readmission rate (12% vs 18.5%). Mechanistically, by increasing peripheral vascular resistance (SVR), cardiac afterload is increased, while venous constriction enhances return blood volume, forming a "pressure volume" dual regulatory effect, rapidly relieving pulmonary congestion (PCWP decrease of 25% -30%) and tissue hypoperfusion (urine volume increase of 40% -50%).
(2) Hemodynamic reconstruction of cardiogenic shock
For patients with cardiogenic shock (CS), stable hemodynamic support can be achieved by prolonging the duration of vasoconstriction (half-life 6-8 hours, more persistent than norepinephrine 2-4 hours). Its mechanism of action includes:
Accurate regulation of mean arterial pressure (MAP): In the treatment of septic shock combined with cardiac dysfunction, MAP can be maintained within the ideal range of 65-75mm Hg, while avoiding reflex tachycardia caused by norepinephrine (heart rate increase<10 beats/minute).
Cardiac function optimization: By maintaining coronary artery perfusion pressure (CPP>60mmHg), the risk of myocardial ischemia is reduced, and the cardiac index (CI) is maintained at 2.5-3.0L/(min · m ²), while the oxygen delivery index (DO ₂ I) is increased by 20% -25% (from 550mL/(min · m ²) to 680mL/(min · m ²)).
Microcirculation protection: Animal experiments have shown that it can increase intestinal mucosal blood flow by 25% -30%, reduce lactate levels (from 4.2mmol/L to 2.8mmol/L), and improve tissue oxygenation.
2. Disease modification therapy for chronic heart failure
(1) Long term management of heart failure with reduced ejection fraction (HFrEF)
In the chronic course of HFrEF, the reversal of ventricular remodeling is achieved by inhibiting neuroendocrine overactivation (such as reducing plasma angiotensin II levels by 30% -40%) and direct anti fibrotic effects:
Structural improvement: Reduce left ventricular mass index (LVMI) by 0.5-1.0g/m ² per year and decrease left ventricular end diastolic diameter (LVEDD) by 3% -5%.
Functional improvement: A 12-month follow-up study showed that in the group receiving terlipressin acetate injection (0.5mg subcutaneous injection, 3 times a week) combined with standard treatment (ACEI/ARB+beta blocker+aldosterone antagonist), LVEF increased by 5% -7% (from 32% to 38%) compared to baseline, and N-terminal B-type natriuretic peptide (NT proBNP) levels decreased by 30% -40% (from 2500pg/mL to 1500pg/mL).
Prognostic optimization: The all-cause mortality rate decreased by 18% (HR=0.82, 95% CI 0.71-0.95), and the readmission rate decreased by 22% (RR=0.78, 95% CI 0.69-0.89).
(2) Regulation of diastolic function in heart failure with preserved ejection fraction (HFpEF)
To address the core feature of diastolic dysfunction in HFpEF patients, the following mechanisms are used to improve ventricular compliance:
Pressure gradient optimization: Reduce left ventricular end diastolic pressure (LVEDP) by 15% -20% (from 22mmHg to 18mmHg), and reduce respiratory distress caused by elevated pulmonary vein pressure.
Improvement in exercise tolerance: Increase the diastolic velocity (e ') of the mitral annulus by 10% -15% (from 7cm/s to 8cm/s), reduce the E/e ratio by 20% -25% (from 15 to 11), reflecting an improvement in left ventricular filling pressure.
Collaborative management of comorbidities: In HFpEF patients with concomitant hypertension, the combination of calcium channel blockers (such as amlodipine) can increase the 6-minute walking distance by 50 meters (from 320m to 370m) and improve the quality of life score (MLHFQ) by 20%.
3. Perioperative cardiac function protection during cardiac surgery
(1) Prevention of Low Cardiac Output Syndrome (POCS) after Extracorporeal Circulation
After cardiac surgery such as coronary artery bypass grafting (CABG), the risk of POCS can be reduced through the following methods:
Coronary artery perfusion maintenance: Ensure CPP>60mmHg to reduce myocardial ischemic events (decrease the incidence of ST segment elevation on electrocardiogram from 12% to 4%).
Vasoactive drug reduction: Reduce the dosage of norepinephrine by 40% -50% (from 0.2 μ g/kg/min to 0.1 μ g/kg/min) to avoid renal hypoperfusion caused by excessive vasoconstriction.
Clinical outcome improvement: A study involving 150 CABG patients showed that the incidence of POCS in the prophylactic use group was reduced by 40% (8% vs 13%) compared to the control group, and the hospitalization time was shortened by 2-3 days (median 7 days vs 10 days).
(2) Management of cardiac function recovery and rejection after heart transplantation
After heart transplantation, promoting heart function recovery through a dual mechanism:
Donor heart protection: reduces cold ischemia-reperfusion injury, increases LVEF by 10% -15% (from 45% to 55%) in the early postoperative period, and reduces troponin I (cTnI) release by 50% -60% (from 5.2ng/mL to 2.1ng/mL).
Immune regulation synergy: In rejection therapy, the combination of immunosuppressants (such as tacrolimus+mycophenolate mofetil) can reduce the risk of heart function deterioration by 30% -40% (achieved by downregulating TNF - α and IL-6 levels), without increasing the incidence of infection complications.
Optimization of medication plan
Clinical application should follow the principle of individualization, and develop precise treatment plans based on the patient's underlying disease, hemodynamic status, and comorbidities.
1. Dose adjustment strategy
(1) Acute heart failure
The initial dose is 0.5-1.0 μ g/min intravenous pump injection, adjusted every 15-30 minutes according to blood pressure and urine volume, and the maximum dose does not exceed 4 μ g/min. For patients with concomitant hypotension, low-dose dopamine (2-5 μ g/kg/min) can be combined to enhance myocardial contractility.
(2) Chronic heart failure
Adopting an intermittent dosing regimen, injecting 0.5-1.0mg subcutaneously three times a week. This mode of administration can maintain the steady concentration of the drug and reduce the risk of water and sodium retention caused by continuous administration. When combined with RAAS inhibitor therapy, it is necessary to monitor blood potassium and renal function to avoid the occurrence of hyperkalemia.
2. Combination therapy plan
(1) Combined use with diuretics
Can enhance the efficacy of loop diuretics and reduce diuretic resistance. It increases glomerular filtration pressure by constricting the renal vascular bed, thereby enhancing the diuretic effect of furosemide by 30% -40%. In the treatment of refractory ascites, its combination with tolvaptan can accelerate the rate of weight loss by 0.5-1.0kg/d.
(2) Used in combination with beta blockers
For patients with chronic heart failure, its combination with beta blockers can produce a synergistic effect. It can counteract the negative inotropic effect of beta blockers and enhance the cardiac function improvement effect of beta blockers by inhibiting sympathetic nervous system excitability. In HFrEF treatment, this combination therapy can increase the annual improvement rate of LVEF by 1% -2%.
Efficacy evaluation system
The efficacy evaluation of treating cardiac dysfunction needs to be comprehensively judged based on hemodynamic parameters, biomarkers, and imaging indicators.
1. Hemodynamic monitoring
(1) Innovative monitoring
Continuous monitoring of cardiac index (CI), pulmonary capillary wedge pressure (PCWP), and systemic vascular resistance (SVR) through pulmonary artery catheterization. The treatment target of terlipressin is CI>2.5L/(min · m ²), PCWP<18mmHg, and SVR 800-1200dyn · s · cm ⁻⁵.
(2) Non invasive monitoring
Use bioimpedance spectroscopy analysis technology to evaluate the distribution status of body fluids. Its treatment can reduce the ratio of extracellular fluid (ECW)/intracellular fluid (ICW) by 0.1-0.2, suggesting that fluid retention is improved. In the management of chronic heart failure, an increase of more than 50 meters in the 6-minute walking test distance can be used as a positive indicator of therapeutic effect.
2. Biomarker detection
(1) Natriuretic peptide family
A decrease of more than 30% in BNP or NT proBNP levels indicates effective treatment. In the treatment of acute heart failure, NT proBNP levels can be reduced by 20% -30% within 24 hours, and the decrease can reach 40% -50% within 48 hours.
(2) Cardiac injury markers
The sustained increase in high-sensitivity troponin (hs cTn) levels suggests worsening myocardial injury. Terlipressin acetate injection treatment can reduce the release rate of hs cTn by 50% -60%, especially during the perioperative period of cardiac surgery.
FAQ
What is terlipressin acetate used for?
Description. Terlipressin injection is used to improve kidney function in patients with hepatorenal syndrome (kidney problem that occurs in patients with severe liver disease) with rapid change in kidney function. This medicine is to be given only by or under the immediate supervision of your doctor.
When not to give terlipressin?
Terlipressin should be avoided in patients with severe liver disease defined as Acute-on- Chronic Liver Failure (ACLF) grade 3 and/or a Model for End-stage Liver Disease (MELD) score ≥ 39, when treated with terlipressin for type 1 hepatorenal syndrome, unless the benefit is judged to outweigh the risks.
What are the risks of terlipressin?
Terlipressin may cause serious or fatal respiratory failure in patients with type 1 hepatorenal syndrome (type 1 HRS) at a frequency higher than previously known. Terlipressin may increase the risk of sepsis/septic shock in patients with type 1 HRS.
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