Art. -Nr.: HY-12341

Onvoloxastat

Name: Onvoloxastat
Brand: MedChemExpress
SKU: HY-12341
Price: 120.00 USD
Availability: InStock
Rating: 5 (9 reviews)

(Synonyms: ML355)

9 Cited Publications

Kundenbewertung

Based on 9 publication(s) in Google Scholar

Onvoloxastat (ML355) is an orally active selective 12-LOX inhibitor with an IC₅₀ of 0.34 μM. Onvoloxastat inhibits platelet activation by blocking thrombin- or thromboxane A2-induced phosphorylation of Akt, PI3K and Erk1/2. At low doses (1-20 μM), it mainly acts by reducing ROS levels, while at high doses (50 μM), it functions via activating the cAMP pathway. Onvoloxastat can be used in research related to thrombosis and diabetes.

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Reinheit : 98.11%
CAS. Nr.: 1532593-30-8
Formel: C₂₁H₁₉N₃O₄S₂
Molecular Weight:441.52

Speicherung:

Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 1 year , -20°C, 6 months

Onvoloxastat Chemical Structure

CAS. Nr.: 1532593-30-8

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Top Publications Citing

Use of MCE Products

Fluorescent Dye

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biologische Aktivität
- Beschreibung
- IC₅₀ & Target
- In Vitro
- Parmacokinetics
- In Vivo
Chemical Information
Publications (9)
Lösungsmittel & Löslichkeit
- In Vitro
- In Vivo
Protokoll (5)
Reinheit & Dokumentation
Verweise
Help & FAQs
Classifications
Bioz

Biologische Aktivität

Beschreibung

IC₅₀ & Target

^[1]

12-LOX

0.34 μM (IC₅₀)

Alle Lipoxygenase Isoform-spezifische Produkte anzeigen :

Alle Akt Isoform-spezifische Produkte anzeigen :

Alle PI3K Isoform-spezifische Produkte anzeigen :

Alle ERK Isoform-spezifische Produkte anzeigen :

In Vitro

Onvoloxastat (ML355) (1-50 μM; 40 min) dose-dependently inhibits αIIbβ3 integrin activation in washed human platelets induced by Thrombin (HY-114164) and U46619 (HY-108566)^[1].

Onvoloxastat (50 μM; 1-60 min) inhibits fibrinogen binding in a time-dependent manner in washed human platelets^[1].
Onvoloxastat (1-50 μM; 30 min) induces cAMP-dependent phosphorylation of VASP at Ser157 and Ser239 in washed human platelets without affecting cell viability^[1].

Onvoloxastat (0.1-100 μM; 10 min) does not directly affect cGMP-producing activity in recombinant human GC-1 enzyme^[1].
Onvoloxastat (25-100 μM; 5 min) dose-dependently inhibits platelet aggregation induced by Thrombin, PAR1-AP, PAR4-AP (HY-P1309) and Collagen (HY-NP003), and reduces 12-HETE production in washed human platelets^[2].

Onvoloxastat (25-100 μM; pre-incubated for 5 min) attenuates platelet adhesion, aggregation and thrombosis in human whole blood^[2].
Onvoloxastat (1 pM-100 μM; 4 h) inhibits AA/IONO-stimulated 12-HETE production in mouse pancreatic islet β cells (BTC3)^[3].
Onvoloxastat (10 μM; 30 min) inhibits AA/IONO-induced 12-HETE expression in human primary islet cells^[3].
Onvoloxastat (1-50 μM; 30 min) dose-dependently blocks the phosphorylation of Akt, PI3K and Erk1/2 and reduces reactive oxygen species (ROS) levels in thrombin-activated washed human platelets, but does not affect p38 phosphorylation. It does not inhibit platelet activation in Crp-XL-activated washed human platelets^[1].

Onvoloxastat (1-50 μM; 60 min) dose-dependently inhibits ABT-737 (HY-50907)-induced phosphatidylserine (PS) externalization and Caspase-3 cleavage in washed human platelets^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.

Western Blot Analysis^[1]

View Protocol

Cell Line:

Washed human platelets
Concentration:

1, 10, 20, 50 μM
Incubation Time:

30 min
Result:

Blocked thrombin-induced PI3K, Akt, and Erk1/2 phosphorylation, but did not affect p38 kinase phosphorylation.
Did not inhibit Crp-XL-induced Syk and PLCγ2 phosphorylation, and enhanced the phosphorylation signals at the 50 μM dose.
Induced cAMP-dependent VASP phosphorylation at Ser157 and Ser239.

Cell Viability Assay^[1]

View Protocol

Cell Line:

Washed human platelets
Concentration:

1, 10, 20, 50 μM
Incubation Time:

30 min
Result:

Did not affect the viability signal of the platelets.

Apoptosis Analysis^[1]

View Protocol

Cell Line:

Washed human platelets
Concentration:

1, 10, 20, 50 μM
Incubation Time:

60 min
Result:

Dose-dependently blocked ABT-737-induced phosphatidylserine (PS) exposure on the platelet surface.

Western Blot Analysis^[1]

View Protocol

Cell Line:

Washed human platelets
Concentration:

1, 10, 20, 50 μM
Incubation Time:

60 min
Result:

Prevented ABT-737-induced Caspase-3 cleavage.

ELISA Assay^[1]

View Protocol

Cell Line:

Mouse beta cells (BTC3)
Concentration:

1 pM, 0.01 μM, 0.1 μM, 1 μM, 10 μM, 100 μM
Incubation Time:

4 h
Result:

Dose-dependently inhibited AA/IONO-stimulated 12-HETE production.

ELISA Assay^[1]

View Protocol

Cell Line:

Human primary donor islets
Concentration:

10 μM
Incubation Time:

30 min
Result:

Inhibited AA/IONO-induced 12-HETE levels.

Parmacokinetics

Species	Dose	Route	C_max	T_1/2	AUC_inf	V_d	CL	F
Mice^[2]	30 mg/kg	p.o.	57 μM	/	/	/	/	/
Mice^[4]	30 mg/kg	p.o.	/	2.9 h	38 μM	0.55 L/kg	3.4 mL/min/kg	20 %

In Vivo

Onvoloxastat (ML355) (1.5 mg/kg; i.v.; single dose; 24 h pretreatment) delays vascular occlusion in the FeCl₃(HY-Y0266)-induced carotid artery thrombosis model^[1].
Onvoloxastat (1.5 mg/kg; i.v.; single dose; 24 h pretreatment) inhibits platelet recruitment and thrombus growth in a laser-induced cremaster muscle microartery thrombosis model^[1].
Onvoloxastat (1.5 mg/kg; i.v.; single administration; 24 h pre-treatment) does not impair normal hemostatic function, prolong bleeding time, or increase blood loss in the tail-clip bleeding model and thromboelastography assay^[1].
Onvoloxastat (15-30 mg/kg; i.g.; twice daily; for 2 consecutive days) inhibits thrombus growth and significantly delays the time to complete vascular occlusion in a ferric chloride FeCl₃-induced mesenteric arteriolar thrombosis model in wild-type mice^[2].
Onvoloxastat (1.88-30 mg/kg; i.g.; twice daily; for 2 consecutive days) potently inhibits thrombosis in a laser-induced cremasteric arteriole thrombosis model in WT mice^[2].
Onvoloxastat (15 mg/kg; i.g.; twice daily; for 2 consecutive days; recorded for 5 minutes after laser injury, with repeated injuries at 5- and 10-minute intervals) exerts no significant effect on hemostatic plug formation and platelet plug dynamics in the laser-ablated saphenous vein hemostasis model of WT mice^[2].
Onvoloxastat (15 mg/kg; i.g.; twice daily; for 2 consecutive days) does not alter microvascular hemostasis time in laser-induced cremaster muscle microvascular rupture and plasma extravasation models of WT mice^[2].

Onvoloxastat (3.5-30 mg/kg; i.g.; twice daily; for 2 consecutive days) does not significantly prolong tail bleeding time or increase total red blood cell loss in the tail amputation bleeding model of WT mice^[2].

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

Animal Model:

C57BL/6 wild-type mice (male,10-12 weeks old) laser-induced cremaster arteriole thrombosis model^[1]
Dosage:

1.5 mg/kg
Administration:

i.v.; single dose; 24 h pretreatment
Result:

Reduced dynamic platelet accumulation and recruitment within the thrombus at the injury site.

Animal Model:

C57BL/6 wild-type mice (male,10-12 weeks old) FeCl₃-induced carotid artery thrombosis model^[1]
Dosage:

1.5 mg/kg
Administration:

i.v.; single dose; 24 h pretreatment
Result:

Delayed the growth rate of thrombus in the carotid artery.
Significantly prolonged the time to complete vessel occlusion.

Animal Model:

C57BL/6 wild-type mice (male,10-12 weeks old) tail bleeding model and thromboelastography (TEG) coagulation test^[1]
Dosage:

1.5 mg/kg
Administration:

i.v.; single dose; 24 h pretreatment
Result:

Did not cause significant alterations in coagulation parameters.
Did not significantly prolong tail bleeding time or increase total hemoglobin loss.

Animal Model:

C57BL/6 wild-type mice (male,10-12 weeks old) FeCl₃-induced mesenteric arteriole thrombosis (topical application of 30 μL of 250 mM FeCl3 solution)^[2]
Dosage:

15, 30 mg/kg
Administration:

i.g.; twice daily; for 2 consecutive days
Result:

Severely impaired platelet adhesion, aggregation, and thrombus formation; the formed thrombi were unstable and frequently embolized
Significantly delayed the time to complete vessel occlusion in mesenteric arterioles, with some mice failing to occlude within 40 minutes.

Animal Model:

C57BL/6 wild-type mice (male,10-12 weeks old) laser-induced cremaster arteriole thrombosis model^[2]
Dosage:

1.88, 3.75, 7.5, 15, 30 mg/kg
Administration:

i.g.; twice daily; for 2 consecutive days
Result:

Strongly inhibited platelet recruitment and fibrin formation at the injury site; thrombi were smaller, unstable, and detached more readily.
At moderate doses (3.75, 7.5 mg/kg), significantly inhibited platelet recruitment, but fibrin content was not significantly.
At the lowest dose (1.88 mg/kg), platelet recruitment and fibrin content were comparable to the control group.

Animal Model:

C57BL/6 wild-type mice (male,10-12 weeks old) laser ablation saphenous vein hemostasis model (puncturing the vessel wall)^[2]
Dosage:

15 mg/kg
Administration:

i.g.; twice daily; for 2 consecutive days
Result:

Did not significantly alter hemostatic plug formation at the site of vascular injury.
Under repeated injury stimulation, the dynamics of the platelet plug and fibrin formation within the hemostatic clot did not significantly differ compared to the control group.

Animal Model:

C57BL/6 wild-type mice (male,10-12 weeks old) laser-induced cremaster microvasculature (arteriole/venule) rupture plasma extravasation model^[2]
Dosage:

15 mg/kg
Administration:

i.g.; twice daily; for 2 consecutive days
Result:

Showed no notable difference in plasma (fluorescent dextran) extravasation or the time required for cessation of extravasation after platelet plug formation compared to controls.

Animal Model:

C57BL/6 wild-type mice (male,10-12 weeks old) tail-bleeding model (transection of 5mm of the distal tail, submerged in warm saline)^[2]
Dosage:

3.5, 15, 30 mg/kg
Administration:

i.g.; twice daily; for 2 consecutive days
Result:

Did not significantly prolong the tail bleeding time of the mice.
Did not increase the total amount of red blood cell loss.

Chemical Information

CAS. Nr. 1532593-30-8
Appearance Solid
Molecular Weight 441.52
Formel C₂₁H₁₉N₃O₄S₂
Color White to gray
SMILES

O=S(NC1=NC2=CC=CC=C2S1)(C3=CC=C(NCC4=CC=CC(OC)=C4O)C=C3)=O
Synonyms

ML355
Versand

Room temperature in continental US; may vary elsewhere.

Speicherung

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	1 year
	-20°C	6 months

Publications (9)

All Flow CytometryOthersWB

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Journal Impact Factor

Nat Med

An ALOX12-12-HETE-GPR31 signaling axis is a key mediator of hepatic ischemia-reperfusion injury. [Abstract]

2018 Jan;24(1):73-83. PMID: 29227475

Onvoloxastat purchased from MedChemExpress. Usage Cited in: Nat Med. 2018 Jan;24(1):73-83. [Abstract]

The phosphorylated and total levels of p65, JNK, p38 and ERK in primary hepatocytes treated with ML355 (10 μM) under normoxia (Nor) or hypoxia (Hyp) conditions. For western blot analysis, GAPDH served as a loading control.
Cell Metab

Pharmacological inhibition of arachidonate 12-lipoxygenase ameliorates myocardial ischemia-reperfusion injury in multiple species. [Abstract]

2021 Oct 5;33(10):2059-2075.e10. PMID: 34536344
Nat Commun

A mouse protozoan boosts antigen-specific mucosal IgA responses in a specific lipid metabolism- and signaling-dependent manner. [Abstract]

2024 Sep 10;15(1):7914. PMID: 39256385

Onvoloxastat purchased from MedChemExpress. Usage Cited in: Nat Commun. 2024 Sep 10;15(1):7914. [Abstract]

Starting from day 6, mice were administered the carrier and ML-355 (15 mg/kg) daily via oral gavage. On day 7, mice were challenged by intraperitoneal injection of OVA+CFA. On day 21, the relative levels of anti-OVA IgA in serum and cecal contents were measured.
Cell Commun Signal

Cytochrome P450 1A1 enhances inflammatory responses and impedes phagocytosis of bacteria in macrophages during sepsis. [Abstract]

2020 May 4;18(1):70. PMID: 32366266
Phytomedicine

Baicalein alleviates cisplatin-induced acute kidney injury by inhibiting ALOX12-dependent ferroptosis. [Abstract]

2024 Jul 25:130:155757. PMID: 38805781
Free Radic Biol Med

CX-5461 ameliorates disease in lupus-prone mice by triggering B-cell ferroptosis via p53-SLC7A11-ALOX12 pathway. [Abstract]

2024 Oct:223:325-340. PMID: 39111584

Onvoloxastat purchased from MedChemExpress. Usage Cited in: Free Radic Biol Med. 2024 Oct:223:325-340. [Abstract]

Selected Raji cells were treated with 1 μM CX-5461, with or without 10 μM ML355, and lipid ROS levels were analyzed by flow cytometry. Representative results and quantitative analyses are presented.
Int Immunopharmacol

Palmitic acid inhibits macrophage-mediated chemotherapy resistance in multiple myeloma via ALOX12 signaling. [Abstract]

2024 Oct 7;143(Pt 1):113320. PMID: 39378653
Inflammation

MAGL Inhibition Relieves Psoriasiform Inflammation and Pruritus Via Modulation of ALOX12-12-HETE Axis in Mice. [Abstract]

2026 Mar 3;49(1):92. PMID: 41774275
Transl Cancer Res

2026 Jul 31;15(7):555. PMID: 42591750

Lösungsmittel & Löslichkeit

In Vitro:

DMSO : ≥ 42 mg/mL (95.13 mM; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

* "≥" means soluble, but saturation unknown.

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

2.2649 mL

11.3245 mL

22.6490 mL

5 mM

0.4530 mL

2.2649 mL

4.5298 mL

10 mM

0.2265 mL

1.1325 mL

2.2649 mL

Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.

Storage method and period of stock solution: -80°C, 1 year; -20°C, 6 months. When stored at -80°C, please use it within 1 year. When stored at -20°C, please use it within 6 months.

Molaritätsrechner

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Konzentration Konzentration

Volumen Volumen

Molecular Weight Molecular Weight

Verdünnungsrechner

Konzentration _{(Stammlösung)} × Volumen _{(Stammlösung)} = Konzentration _{(Ziellösung)} × Volumen _{(Ziellösung)}

Konzentration _{(Stammlösung)} Konzentration _{(Stammlösung)}

Volumen _{(Stammlösung)} Volumen _{(Stammlösung)}

Konzentration _{(Ziellösung)} Konzentration _{(Ziellösung)}

Volumen _{(Ziellösung)} Volumen _{(Ziellösung)}

In Vivo:

Select the appropriate dissolution method based on your experimental animal and administration route.

Stock Solution Working Solution

For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

Protocol 1

Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline

Solubility: ≥ 2.5 mg/mL (5.66 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.

Protocol 2

Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)

Solubility: ≥ 2.5 mg/mL (5.66 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

Protocol 3

Add each solvent one by one: 10% DMSO 90% Corn Oil

Solubility: ≥ 2.5 mg/mL (5.66 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL Corn oil, and mix evenly.

Protocol 4

Add each solvent one by one: 5% DMSO 95% (20% SBE-β-CD in Saline)

Solubility: ≥ 2.5 mg/mL (5.66 mM); Clear solution

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

Dosage Dosage
mg/kg
Animal Weight (Per Animal) Animal Weight (Per Animal)
g
Dosing Volume (Per Animal) Dosing Volume (Per Animal)
μL
Number of Animals Number of Animals

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Please enter your animal formula composition:

%
DMSO +

Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
%
+
+
%
Tween-80 + +
%
Saline +

The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).

Working solution concentration: 0.22 mg/mL

Protokoll

All Signal Pathway Related Molecular Biology Cell Biology

Kinase activity and phosphorylation assays
Kinase activity assays measure the ability of kinases to transfer phosphate groups from ATP to specific substrates, while phosphorylation assays detect the presence and levels of phosphorylated proteins. Common methods include radiolabeled ATP incorporation (e. g. ,), ADP release detection via bioluminescence (e. g. ,[3]), enzyme-linked immunosorbent assays (ELISA) for phospho-specific epitopes (e. g. ,[6]), and microtiter-based formats for high-throughput screening (e. g. ,[8]). The ADP-Glo assay quantifies kinase activity by measuring ADP produced during phosphorylation using a luciferase-based system. Radiometric assays involve autoradiography or scintillation counting after incorporation of ³²P-labeled ATP into substrate proteins. ELISA-based approaches rely on phospho-specific antibodies to detect activated kinases in cell lysates or purified samples.
Western Blot
Western blotting (WB) is a commonly used experimental method in molecular biology, biochemistry, and immunogenetics for identifying and quantifying target proteins. It combines gel electrophoresis with immunoassay, enabling researchers to analyze protein expression, post-translational modifications, and molecular weight.
ROS/oxidative-stress fluorescent staining
ROS/oxidative-stress fluorescent staining uses cell-permeant fluorogenic probes that become fluorescent after oxidation inside cells or tissues; commonly used examples include DCFH-DA/DCFDA for broad cellular oxidant detection, DHE for superoxide-related signal detection, MitoSOX for mitochondrial superoxide-related signal detection, and CellROX probes for oxidative-stress-associated fluorescence readouts. The assay detects probe oxidation rather than a single ROS species unless the probe and analysis method have been chemically validated for that species. DCFH-DA enters cells, is deacetylated by intracellular esterases to DCFH, and produces fluorescent DCF after oxidation, so the readout is used as an operational measure of total cellular oxidative stress rather than a species-specific ROS measurement. DHE and MitoSOX can report superoxide-related oxidation, but red fluorescence alone can include non-specific ethidium-like oxidation products; HPLC or optimized spectral approaches are
Protocol for Kinase activity and phosphorylation assays
Kinase activity assays measure transfer of phosphate from ATP to a protein or peptide substrate, generating phosphorylated substrate, ADP, or incorporated radiolabeled phosphate as the readout; phosphorylation assays measure site-specific phosphorylation in cells or tissues as a proxy for kinase-pathway activation, inhibition, or substrate regulation. Phosphorylation can be detected by phospho-specific Western blot, immunoprecipitation kinase assay, phospho-immunofluorescence, phospho-flow cytometry, luminescent ADP detection, radiolabeled ATP incorporation, or reporter-based pathway assays, and these readouts can be applied to cancer cells, primary neurons, mouse tumors, organoids, inflammatory macrophages, ferroptosis studies, and mitophagy studies when the kinase target is biologically relevant.
Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked

Reinheit & Dokumentation

Select Batch:

Reinheit: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (306 KB)
SDS (393 KB)
- English - EN (393 KB)
- Français - FR (393 KB)
- Deutsch - DE (393 KB)
- Norwegian - NO (393 KB)
- Español - ES (393 KB)
- Swedish - SV (393 KB)
- Italian - IT (393 KB)
- Korean - KR (393 KB)
- Portuguese - PT (393 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

Verweise

[1]. Shpakova V, et al. ML355 Modulates Platelet Activation and Prevents ABT-737 Induced Apoptosis in Platelets. The Journal of pharmacology and experimental therapeutics. 2022 May;381(2):164-175.

[2]. Adili R, et al. First Selective 12-LOX Inhibitor, ML355, Impairs Thrombus Formation and Vessel Occlusion In Vivo With Minimal Effects on Hemostasis. Arteriosclerosis, thrombosis, and vascular biology. 2017 Oct;37(10):1828-1839. [Content Brief]

[3]. Luci D, et al. Discovery of ML355, a Potent and Selective Inhibitor of Human 12-Lipoxygenase. 2013 Apr 12 [updated 2014 Sep 18]. In: Probe Reports from the NIH Molecular Libraries Program [Internet]. Bethesda (MD): National Center for Biotechnology Information (US); 2010–. PMID: 25506969

[4]. Pizzorno J, et al. Health Medicine. Integrative medicine (Encinitas, Calif.). 2022 Dec;21(6):8-14. [Content Brief]

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

Storage method and period of stock solution: -80°C, 1 year; -20°C, 6 months. When stored at -80°C, please use it within 1 year. When stored at -20°C, please use it within 6 months.

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	2.2649 mL	11.3245 mL	22.6490 mL	56.6226 mL
	5 mM	0.4530 mL	2.2649 mL	4.5298 mL	11.3245 mL
	10 mM	0.2265 mL	1.1325 mL	2.2649 mL	5.6623 mL
	15 mM	0.1510 mL	0.7550 mL	1.5099 mL	3.7748 mL
	20 mM	0.1132 mL	0.5662 mL	1.1325 mL	2.8311 mL
	25 mM	0.0906 mL	0.4530 mL	0.9060 mL	2.2649 mL
	30 mM	0.0755 mL	0.3775 mL	0.7550 mL	1.8874 mL
	40 mM	0.0566 mL	0.2831 mL	0.5662 mL	1.4156 mL
	50 mM	0.0453 mL	0.2265 mL	0.4530 mL	1.1325 mL
	60 mM	0.0377 mL	0.1887 mL	0.3775 mL	0.9437 mL
	80 mM	0.0283 mL	0.1416 mL	0.2831 mL	0.7078 mL

Bioz

Onvoloxastat

9 Cited Publications

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Onvoloxastat

Publications Citing Use of MedChemExpress (MCE) Onvoloxastat

Alle Lipoxygenase Isoform-spezifische Produkte anzeigen

Alle Akt Isoform-spezifische Produkte anzeigen

Alle PI3K Isoform-spezifische Produkte anzeigen

Alle ERK Isoform-spezifische Produkte anzeigen