| Size | Price | Stock | Qty |
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| 5mg |
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| 10mg |
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| 25mg |
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| 50mg |
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| 100mg |
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| 250mg |
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| 500mg |
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| Other Sizes |
Purity: = 99.58%
| Targets |
vasopressin V1 receptor
Terlipressin acetate targets vasopressin receptors, primarily the V1A receptor. It acts as a partial agonist at the vasopressin V1A receptor with a Ki of 0.85 µM. The compound is also an agonist of human V1, V2, and V1B receptors. By activating V1 receptors on vascular smooth muscle, terlipressin causes vasoconstriction, reducing splanchnic blood flow and portal pressure. The V2 receptor agonism contributes to its effects on water reabsorption and renal function. |
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| ln Vitro |
In vitro, terlipressin acetate demonstrates potent vasoactive properties. It acts as a partial agonist at the vasopressin V1A receptor with a binding affinity (Ki) of 0.85 µM. The compound shows selectivity for V1 receptors over other vasopressin receptor subtypes. In cell-based assays, terlipressin activates downstream signaling pathways including phospholipase C and calcium mobilization, leading to vascular smooth muscle contraction.
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| ln Vivo |
In vivo, terlipressin acetate reduces splanchnic blood flow and portal pressure, thereby controlling acute variceal bleeding. It is used clinically as a vasoactive drug in the management of low blood pressure. The compound is effective in treating acute esophageal variceal hemorrhage (EVH) and hepatorenal syndrome. It has also been investigated for its anti-inflammatory and antioxidant effects and for use in norepinephrine-resistant septic shock.
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| Enzyme Assay |
In vitro receptor binding assays for terlipressin measure its affinity for vasopressin V1A, V1B, and V2 receptors using radioligand displacement techniques. Membranes prepared from cells expressing the receptor are incubated with a radiolabeled vasopressin analog and varying concentrations of terlipressin. The binding affinity (Ki) is calculated from competitive binding curves. For functional assays, receptor activation is measured by calcium mobilization or cAMP accumulation in cells expressing the respective receptors.
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| Cell Assay |
In vitro cell-based assays for terlipressin use cell lines expressing vasopressin receptors. For V1 receptor activity, cells are treated with terlipressin and intracellular calcium levels are measured using fluorescent indicators. For V2 receptor activity, cAMP accumulation is quantified by ELISA or radioimmunoassay. The EC50 for receptor activation is calculated from dose-response curves. These assays confirm the compound's agonist activity and receptor selectivity profile.
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| Animal Protocol |
In vivo animal models for terlipressin include rat models of portal hypertension and variceal bleeding. The compound is administered intravenously, and its effects on portal pressure, splanchnic blood flow, and systemic hemodynamics are measured. Efficacy in controlling bleeding is assessed in models of gastrointestinal hemorrhage. Pharmacodynamic studies evaluate the dose-response relationship and duration of action. The compound's effects on renal function are assessed in models of hepatorenal syndrome.
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| ADME/Pharmacokinetics |
Absorption, Distribution and Excretion
In HRS-1 patients, following intravenous administration of 1 mg terlipressin acetate, the median Cmax, AUC24h, and Cave at steady state for terlipressin were 70.5 ng/mL, 123 ng × hr/mL, and 14.2 ng/mL, respectively. The median Cmax, AUC24h, and Cave for lisiopressin were 1.2 ng/mL, 11.2 ng × hr/mL, and 0.5 ng/mL, respectively. Both terlipressin and lisiopressin exhibited linear pharmacokinetic characteristics in healthy subjects. Plasma concentrations of terlipressin increased proportionally to the administered dose. Less than 1% of terlipressin and less than 0.1% of lysine vasopressin were excreted in the urine of healthy subjects. The volume of distribution for terlipressin was 6.3 L, and for lysine vasopressin, it was 1370 L. Terlipressin has a clearance rate of 27.4 L/hr, while lysine vasopressin has a clearance rate of 318 L/hr. In HRS-1 patients, terlipressin clearance increases with body weight, while body weight has no effect on lysine vasopressin clearance. Metabolism/Metabolites: The N-terminal glycyl residue of terlipressin is cleaved by various tissue peptidases, releasing its pharmacologically active metabolite, lysine vasopressin (LV). After its formation, LV undergoes various peptidase-mediated metabolic pathways in tissues throughout the body. Terlipressin is not metabolized in blood or plasma. Because peptidases are ubiquitous in human tissues, the metabolism of terlipressin is unlikely to be affected by disease states or other drugs. Biological Half-Life: The terminal half-life of terlipressin is 0.9 hours, and that of lysine vasopressin is 3.0 hours. Terlipressin acetate is administered intravenously as a prodrug. It is slowly converted to the active metabolite, lysine-vasopressin, by enzymatic cleavage of the triglycyl moiety. The compound has a half-life of approximately 40-50 minutes, with a prolonged pharmacological effect due to the sustained release of the active metabolite. It is distributed in the plasma and extracellular fluid, with minimal tissue accumulation. The drug is eliminated primarily via the kidneys. |
| Toxicity/Toxicokinetics |
The toxicity profile of terlipressin acetate includes systemic vasoconstriction, which may lead to ischemic complications, including myocardial ischemia, peripheral ischemia, and mesenteric ischemia. Other adverse effects include hypertension, bradycardia, and electrolyte disturbances. The compound is contraindicated in patients with severe cardiovascular disease. In clinical use, careful monitoring of hemodynamic parameters is required to minimize the risk of ischemic events.
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| References |
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| Additional Infomation |
Pharmacodynamics
Terlipressin mimics the biological effects of endogenous vasopressin, but it exhibits greater selectivity for V1 receptors and a longer half-life. These pharmacokinetic and molecular properties of terlipressin offer several advantages, such as prevention of rebound hypotension after discontinuation and ease of use in patients with limited intravenous access. Terlipressin increases arterial pressure (diastolic, systolic, and mean arterial pressure) and decreases heart rate in patients with hepatorenal syndrome type 1 (HRS-1). In HRS-1 patients, cardiovascular effects are observed within 5 minutes of a single administration of 0.85 mg terlipressin and last for at least 6 hours. The greatest changes in blood pressure and heart rate occur between 1.2 and 2 hours after administration. Terlipressin acetate is approved and marketed in many countries for the treatment of acute esophageal variceal bleeding and hepatorenal syndrome. It is available as an injectable formulation for intravenous administration. The compound is recommended in clinical guidelines for the management of variceal hemorrhage. Its mechanism involves activation of vasopressin V1 receptors, leading to splanchnic vasoconstriction and reduced portal pressure. Research continues into its use in other indications including septic shock. |
| Molecular Formula |
C54H78N16O17S2
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|---|---|
| Molecular Weight |
1287.433
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| Exact Mass |
1346.538
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| Elemental Analysis |
C, 50.38; H, 6.11; N, 17.41; O, 21.13; S, 4.98
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| CAS # |
914453-96-6
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| Related CAS # |
Terlipressin diacetate; 1884420-36-3; Terlipressin; 14636-12-5
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| PubChem CID |
72081
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| Sequence |
Gly-Gly-Gly-Cys-Tyr-Phe-Gln-Asn-Cys-Pro-Lys-Gly-NH2 (Disulfide bridge: Cys4-Cys9)
glycyl-glycyl-glycyl-L-cysteinyl-L-tyrosyl-L-phenylalanyl-L-glutaminyl-L-asparagyl-L-cysteinyl-L-prolyl-L-lysyl-glycinamide (4->9)-disulfide acetic acid; H-Gly-Gly-Gly-Cys(1)-Tyr-Phe-Gln-Asn-Cys(1)-Pro-Lys-Gly-NH2.CH3CO2H |
| SequenceShortening |
GGGCYFQNCPKG
GGGCYFQNCPKG-NH2 (Disulfide bridge: Cys4-Cys9) |
| Appearance |
White to off-white solid powder
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| LogP |
-5.8
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| Hydrogen Bond Donor Count |
16
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| Hydrogen Bond Acceptor Count |
19
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| Rotatable Bond Count |
25
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| Heavy Atom Count |
85
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| Complexity |
2380
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| Defined Atom Stereocenter Count |
8
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| SMILES |
S1C[C@@H](C(N2CCC[C@H]2C(N[C@H](C(NCC(N)=O)=O)CCCCN)=O)=O)NC([C@H](CC(N)=O)NC([C@H](CCC(N)=O)NC([C@H](CC2C=CC=CC=2)NC([C@H](CC2C=CC(=CC=2)O)NC([C@H](CS1)NC(CNC(CNC(CN)=O)=O)=O)=O)=O)=O)=O)=O.OC(C)=O
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| InChi Key |
BYDVFOPTAIPAGA-LCGYVTRFSA-N
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| InChi Code |
InChI=1S/C52H74N16O15S2.C2H4O2/c53-17-5-4-9-31(45(76)60-23-41(57)72)63-51(82)38-10-6-18-68(38)52(83)37-27-85-84-26-36(61-44(75)25-59-43(74)24-58-42(73)22-54)50(81)65-34(20-29-11-13-30(69)14-12-29)48(79)64-33(19-28-7-2-1-3-8-28)47(78)62-32(15-16-39(55)70)46(77)66-35(21-40(56)71)49(80)67-37;1-2(3)4/h1-3,7-8,11-14,31-38,69H,4-6,9-10,15-27,53-54H2,(H2,55,70)(H2,56,71)(H2,57,72)(H,58,73)(H,59,74)(H,60,76)(H,61,75)(H,62,78)(H,63,82)(H,64,79)(H,65,81)(H,66,77)(H,67,80);1H3,(H,3,4)/t31-,32-,33-,34-,35-,36-,37-,38-;/m0./s1
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| Chemical Name |
acetic acid;(2S)-1-[(4R,7S,10S,13S,16S,19R)-19-[[2-[[2-[(2-aminoacetyl)amino]acetyl]amino]acetyl]amino]-7-(2-amino-2-oxoethyl)-10-(3-amino-3-oxopropyl)-13-benzyl-16-[(4-hydroxyphenyl)methyl]-6,9,12,15,18-pentaoxo-1,2-dithia-5,8,11,14,17-pentazacycloicosane-4-carbonyl]-N-[(2S)-6-amino-1-[(2-amino-2-oxoethyl)amino]-1-oxohexan-2-yl]pyrrolidine-2-carboxamide
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| Synonyms |
Gly-Gly-Gly-8-Lys-vasopressin; TGLVP; triglycyl lysine vasopressin; Terlipressin; Terlipressin acetate; trade names: Glypressin; Teripress
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples
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| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 0.7767 mL | 3.8837 mL | 7.7674 mL | |
| 5 mM | 0.1553 mL | 0.7767 mL | 1.5535 mL | |
| 10 mM | 0.0777 mL | 0.3884 mL | 0.7767 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
Link: https://clinicaltrials.gov/ct2/show/NCT01640964
Conditions:Compensated Cirrhosis and Portal Hypertension
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