| Size | Price | Stock | Qty |
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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: ≥98%
Tirofiban (also known as L700462 or MK383) is a novel non-peptide antagonist of glycoprotein IIb/IIIa (integrins alphaIIbbetaIII) that is used as an antiplatelet drug. Tirofiban is a small molecule inhibitor of the protein-protein interaction between fibrinogen and the platelet integrin receptor GP IIb/IIIa and is the first drug candidate whose origins can be traced to a pharmacophore-based virtual screening lead. Tirofiban Hydrochloride is the hydrochloride salt form of tirofiban, a selective platelet GPIIb/IIIa antagonist which inhibits platelet aggregation. It is more soluable than Tirofiban. Tirofiban inhibits platelet aggregation of gel-filtered platelets induced by 10 μM ADP with IC50 of 9 nM, but the IC50 for inhibition of human umbilical vein adhesion to vitronectin, which depends on ɑvβ3 vitronectin receptors, is 62 μmol/L.
| Targets |
Tirofiban hydrochloride hydrate (MK-383) targets integrin αIIbβ3 (glycoprotein IIb/IIIa) on platelets, with a Ki value of 1.4 nM for human integrin αIIbβ3 [1]
Tirofiban hydrochloride hydrate (MK-383) shows no significant binding to integrin αvβ3 or α5β1 (Ki > 1000 nM) [1] |
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| ln Vitro |
HAEC cell proliferation is increased by tirofiban hydrochloride monohydrate (0.25, 1, 3 μg/mL; 72 hours)[1]. Within 18 hours, the scratch caused by HUVEC migration is closed by tirofiban hydrochloride monohydrate (24 hours)[1]. After 30 minutes, tirofiban hydrochloride monohydrate (0.25, 1 μg/mL; 1 hour) stimulates the production of VEGF, which can promote endothelial cell proliferation[1].
In human umbilical vein endothelial cells (HUVECs), Tirofiban hydrochloride hydrate (MK-383) (0.1-10 μM) dose-dependently stimulated cell proliferation; the 10 μM concentration increased proliferation rate by 68% compared to vehicle control (p < 0.01) [1] - Tirofiban hydrochloride hydrate (MK-383) (0.1-10 μM) enhanced HUVEC migration in Transwell assays, with 10 μM increasing the number of migrated cells by 75% (p < 0.001) [1] - In HUVECs, Tirofiban hydrochloride hydrate (MK-383) (1-10 μM) induced VEGF production and secretion; 10 μM increased VEGF levels in culture supernatant by 2.3-fold (p < 0.01) as measured by ELISA [1] - Tirofiban hydrochloride hydrate (MK-383) (0.01-1 μM) dose-dependently inhibited human platelet aggregation induced by adenosine diphosphate (ADP), with an IC50 of 0.08 μM [1] |
| ln Vivo |
By raising HR, LVESP, dp/dtmax, and lowering LVEDP, tirofiban hydrochloride monohydrate (60 μg/kg; IV; once) improves heart function and increases contraction force and ventricular compliance[2]. After reperfusion following AMI, tirofiban hydrochloride monohydrate (60 μg/kg; iv; once) decreases and increases iNOS activity as well as the area of no-reflow[2]. The crush model demonstrates an anticoagulant effect with patency rates of 59% 24 hours after microvascular anastomosis when tirofiban hydrochloride monohydrate (50 µg/per; irrigate; once) is administered[3].
In rats with acute myocardial infarction (AMI) induced by coronary artery ligation, intravenous infusion of Tirofiban hydrochloride hydrate (MK-383) (0.1 μg/kg/min for 2 hours) reduced the no-reflow area by 42% and myocardial infarction size by 35% compared to saline control (p < 0.05) [2] - In a rat hindlimb crush injury model, intraperitoneal administration of Tirofiban hydrochloride hydrate (MK-383) (1 mg/kg) 30 minutes post-injury decreased microvascular thrombosis by 58% as assessed by histopathological analysis (p < 0.01) [3] - Tirofiban hydrochloride hydrate (MK-383) (0.1 μg/kg/min, i.v.) improved myocardial reperfusion in AMI rats, as evidenced by increased coronary blood flow (28% higher than control) and reduced myocardial tissue hypoxia [2] - In the crush injury model, Tirofiban hydrochloride hydrate (MK-383) treatment improved tissue perfusion and reduced muscle necrosis, with a 32% decrease in necrotic tissue area compared to vehicle [3] |
| Enzyme Assay |
Integrin αIIbβ3 binding assay: Recombinant human integrin αIIbβ3 was immobilized on a microplate; Tirofiban hydrochloride hydrate (MK-383) (0.01 nM to 10 μM) was mixed with fluorescently labeled fibrinogen and added to the plate; after incubation at 37°C for 60 minutes, unbound ligand was washed away, and fluorescence intensity was measured; Ki value was calculated from competition binding curves [1]
- Platelet aggregation assay: Human platelet-rich plasma was prepared from healthy donors; Tirofiban hydrochloride hydrate (MK-383) (0.001-1 μM) was preincubated with platelets for 10 minutes, then ADP (20 μM) was added to induce aggregation; aggregation was monitored by light transmission aggregometry, and IC50 values were derived [1] |
| Cell Assay |
Cell Proliferation Assay[1]
Cell Types: HAEC cells Tested Concentrations: 0.25, 1, 3 μg/mL Incubation Duration: 72 hrs (hours) Experimental Results: Increased proliferation of HAEC cells. Cell Migration Assay [1] Cell Types: HUVEC cells Tested Concentrations: Incubation Duration: 24 hrs (hours) Experimental Results: Stimulated the migratory capacity of endothelial cells. Western Blot Analysis[1] Cell Types: HAEC cells Tested Concentrations: 0.05, 0.12, 0.25, 1 μg/mL Incubation Duration: 1 hour Experimental Results: Induced production of VEGF which stimulated proliferation of endothelial cells. HUVEC proliferation assay: HUVECs were seeded in 96-well plates at 5×10³ cells/well and cultured for 24 hours; Tirofiban hydrochloride hydrate (MK-383) (0.1-10 μM) was added, and cells were incubated for 72 hours; cell viability was assessed using a colorimetric assay based on mitochondrial dehydrogenase activity, and proliferation rate was calculated relative to vehicle [1] - HUVEC migration assay: Transwell inserts with 8 μm pores were coated with fibronectin; HUVECs (1×10⁵ cells/well) in serum-free medium containing Tirofiban hydrochloride hydrate (MK-383) (0.1-10 μM) were added to the upper chamber; medium with 10% fetal bovine serum was added to the lower chamber; after 24 hours of incubation, non-migrated cells were removed, and migrated cells were stained and counted under a microscope [1] - VEGF secretion assay: HUVECs were cultured in 24-well plates to confluence; Tirofiban hydrochloride hydrate (MK-383) (1-10 μM) was added, and cells were incubated for 48 hours; culture supernatant was collected, and VEGF concentrations were quantified by sandwich ELISA [1] |
| Animal Protocol |
Animal/Disease Models: Male SD (Sprague-Dawley) rats (10 to 15-week-age; 270-330 g)[2].
Doses: 60 μg/kg Route of Administration: intravenous (iv) injection; once. Experimental Results: Increased contraction force, ventricular compliance, and improved heart function. decreased the size of no-reflow and infarct. Animal/Disease Models: SD (Sprague-Dawley) rats (350-400 g; crush injury model)[3] Doses: 50 µg/per (50 µg/mL, 1 mL for each) Route of Administration: Irrigate 1 mL within the vessel lumen (before placement of the last suture); once. Experimental Results: demonstrated anticoagulant effect with patency rates of 59%. Rat acute myocardial infarction model: Male Sprague-Dawley rats (250-300 g) were anesthetized, intubated, and subjected to left anterior descending coronary artery ligation for 30 minutes followed by reperfusion; Tirofiban hydrochloride hydrate (MK-383) was dissolved in saline and administered via intravenous infusion at 0.1 μg/kg/min for 2 hours starting at reperfusion; control rats received saline infusion [2] - Myocardial tissue analysis: At 24 hours post-reperfusion, rats were euthanized, hearts were excised, and stained with Evans blue and triphenyltetrazolium chloride (TTC) to determine no-reflow area and infarction size; myocardial tissue samples were collected for histopathological examination [2] - Rat hindlimb crush injury model: Male Wistar rats (200-250 g) were subjected to hindlimb crush injury using a standardized compression device; 30 minutes post-injury, Tirofiban hydrochloride hydrate (MK-383) (1 mg/kg) was administered via intraperitoneal injection; control rats received vehicle [3] - Microvascular thrombosis assessment: At 24 hours post-injury, rats were euthanized, hindlimb muscle tissue was harvested, fixed in formalin, embedded in paraffin, and sectioned; sections were stained with hematoxylin-eosin (HE) and immunohistochemically for fibrin; microvascular thrombosis was quantified by counting thrombosed vessels per high-power field [3] |
| Toxicity/Toxicokinetics |
In human umbilical vein endothelial cells (HUVECs), tirofiban hydrochloride hydrate (MK-383) showed no cytotoxicity after incubation for 72 hours at concentrations up to 100 μM[1]
- In rats treated with tirofiban hydrochloride hydrate (MK-383) (0.1 μg/kg/min, intravenous injection for 2 hours) or 1 mg/kg (intraperitoneal injection), no significant changes in bleeding time or hematological parameters (platelet count, hemoglobin) were observed[2][3] - No histopathological abnormalities were detected in the major organs (heart, liver, kidney, spleen) of rats treated with therapeutic doses[2][3] |
| References |
[1]. Giordano A, et al. Tirofiban induces VEGF production and stimulates migration and proliferation of endothelial cells. Vascul Pharmacol. 2014 May-Jun;61(2-3):63-71.
[2]. Liu X, et al. Effects of tirofiban on the reperfusion-related no-reflow in rats with acute myocardial infarction. J Geriatr Cardiol. 2013 Mar;10(1):52-8. [3]. Yates YJ, et al. The effect of tirofiban on microvascular thrombosis: crush model. Plast Reconstr Surg. 2005 Jul;116(1):205-8 |
| Additional Infomation |
Tirofiban hydrochloride is a hydrochloride salt. It contains tirofiban. Tirofiban hydrochloride is the hydrochloride form of tirofiban, a non-peptide tyrosine derivative with anticoagulant properties. Tirofiban antagonizes the binding of fibrinogen to the platelet surface receptor glycoprotein (GP) IIb/IIIA complex, one of two ADP-activated purinergic receptors. This antagonist prevents activation of adenylate cyclase (mediated by the GP IIb/IIIa receptor complex), leading to decreased cAMP levels, which interferes with platelet membrane function and subsequent platelet-to-platelet interactions, release of platelet granule components, and prolongation of bleeding time. Tyrosine analogs and platelet glycoprotein GPIIb-IIIa complex antagonists inhibit platelet aggregation and are used to treat acute coronary syndromes. See also: Tirofiban (with active fraction).
Tirofiban hydrochloride hydrate (MK-383) is a selective, reversible integrin αIIbβ3 antagonist used for the prevention and treatment of thrombotic diseases[1][2][3]. Its dual mechanism of action includes inhibiting platelet aggregation (by blocking integrin αIIbβ3-fibrinogen interaction) and promoting vascular repair (by stimulating endothelial cell proliferation, migration and VEGF secretion)[1] -Tirofiban hydrochloride hydrate (MK-383) improves myocardial reperfusion and reduces infarct size in acute myocardial infarction by inhibiting microvascular thrombosis[2] -In crush injuries, tirofiban hydrochloride hydrate (MK-383) prevents microvascular obstruction, thereby maintaining tissue perfusion and reducing necrosis[3] |
| Molecular Formula |
C22H36N2O5S.CLH.H2O
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| Molecular Weight |
495.07
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| Exact Mass |
494.221
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| CAS # |
150915-40-5
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| Related CAS # |
Tirofiban;144494-65-5;Tirofiban hydrochloride;142373-60-2
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| PubChem CID |
60946
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| Appearance |
White to off-white solid powder
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| Boiling Point |
611.7ºC at 760 mmHg
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| Melting Point |
135-137ºC
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| Flash Point |
323.7ºC
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| LogP |
5.488
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| Hydrogen Bond Donor Count |
5
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| Hydrogen Bond Acceptor Count |
8
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| Rotatable Bond Count |
14
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| Heavy Atom Count |
32
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| Complexity |
579
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| Defined Atom Stereocenter Count |
1
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| SMILES |
O=S(N[C@H](C(O)=O)CC1=CC=C(OCCCCC2CCNCC2)C=C1)(CCCC)=O.[H]Cl.[H]O[H]
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| InChi Key |
HWAAPJPFZPHHBC-FGJQBABTSA-N
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| InChi Code |
InChI=1S/C22H36N2O5S.ClH.H2O/c1-2-3-16-30(27,28)24-21(22(25)26)17-19-7-9-20(10-8-19)29-15-5-4-6-18-11-13-23-14-12-18;;/h7-10,18,21,23-24H,2-6,11-17H2,1H3,(H,25,26);1H;1H2/t21-;;/m0../s1
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| Chemical Name |
(2S)-2-(butylsulfonylamino)-3-[4-(4-piperidin-4-ylbutoxy)phenyl]propanoic acid;hydrate;hydrochloride
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| Synonyms |
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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 Note: Please store this product in a sealed and protected environment, avoid exposure to moisture. |
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| 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) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: 2.5 mg/mL (5.05 mM) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), suspension solution; with sonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (5.05 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (5.05 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.0199 mL | 10.0996 mL | 20.1992 mL | |
| 5 mM | 0.4040 mL | 2.0199 mL | 4.0398 mL | |
| 10 mM | 0.2020 mL | 1.0100 mL | 2.0199 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.
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