Fig. 1 · Structure

Cat. No.: A10101
CAS No.: 475108-18-0
Formula: C₂₂H₁₉ClN₄O₅
Mol. Weight: 454.9

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Other Forms

Form	MW
Tivozanib (AV-951) This page	454.9
Tivozanib hydrate	472.88
Tivozanib hydrochloride hydrate	509.34

Tivozanib (AV-951)

Name: Tivozanib (AV-951)
Brand: Adooq Bioscience
SKU: A10101
Availability: InStock
Rating: 5 (7 reviews)

Cat. No. A10101 CAS 475108-18-0

VEGFR Inhibitor

Tivozanib (AV-951) is an oral VEGF receptor tyrosine kinase inhibitor that is designed to inhibit all three VEGF receptors.

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Biological Activity

Bioactivity / Mechanism

Tivozanib treatment reduced VEGFR2 phosphorylation in OVCAR3, SKOV3 and A2780CP ovarian carcinoma cells at higher tested concentrations (5–20 μM, 48 h). Downstream signaling varied by cell line: ERK1/2 phosphorylation increased in SKOV3 cells. These cellular responses do not define biochemical potency or target selectivity. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Target & Activity

Target	Activity	Value
VEGFR2	IC50	6.5nM
VEGFR3	IC50	15nM
EphB2	IC50	24nM
VEGFR1	IC50	30nM
PDGFRα	IC50	40nM
PDGFRβ	IC50	49nM
c-Kit	IC50	78nM
Tie-2	IC50	78nM
EphB4	IC50	480nM
FGFR1	IC50	530nM
c-Met	IC50	550nM
Abl	IC50	620nM
Src	IC50	960nM
FGFR3	IC50	>1μM
FGFR4	IC50	>1μM
FLT3	IC50	>1μM
EGFR	IC50	>1μM
ErbB2	IC50	>1μM
InsulinReceptor	IC50	>1μM
FAK	IC50	>1μM
ErbB4	IC50	>1μM
IGF-1R	IC50	>1μM
JAK2	IC50	>1μM

23 targets · Scroll to view more

In Vitro Studies

In OVCAR3, SKOV3 and A2780CP ovarian carcinoma cells, 48 h exposure to tivozanib (1–20 μM) reduced MTT-based viability relative to vehicle controls. The experiment used DMSO at no more than 0.1% [v/v]. No tivozanib IC50 is assigned from the plotted data. [1]

Ovarian carcinoma cell viability and VEGFR2 signaling

Cell-based study · OVCAR3, SKOV3 and A2780CP human ovarian carcinoma cells [1]

After 48 h, tivozanib reduced MTT-based viability and, at higher tested concentrations, VEGFR2 phosphorylation. Downstream responses varied by cell line: ERK1/2 phosphorylation increased in SKOV3 cells. These cellular findings do not establish an isolated-enzyme IC50 or target selectivity.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
MTT-based cell viability relative to vehicle-treated controls	Qualitative concentration response Reduced viability; exact percentages and IC50 not extracted	[1]
VEGFR2 phosphorylation and downstream ERK1/2 response	Qualitative immunoblot response Reduced p-VEGFR2 at higher concentrations; increased p-ERK1/2 in SKOV3	[1]

Literature-Reported Treatment Conditions

Treatment concentration: MTT: 1, 2, 5, 10 and 20 μM; immunoblotting: 5, 10 and 20 μM; vehicle controls shown at 0 μM
Exposure duration: 48 h
Method: In vitro exposure followed by MTT or immunoblot analysis
Vehicle: DMSO; final concentration did not exceed 0.1% [v/v]
Co-treatment: Tivozanib alone in the selected experiments
Reported limits: Exact vehicle percentage per condition and batch identity were not specified. No numerical IC50 was extracted for tivozanib.

Methods and source locations

Compound reported in the paper: Tivozanib; Compound label in the paper: Tivozanib (AV-951)

Cellular effects of the named compound in the reported models and conditions only.

Figure 2A and legend; Methods: Cytotoxicity assays, Antibodies and chemicals, Statistical analysis; Figure 5 and legend; Results: Effects of tivozanib on VEGFR2, AKT, ERK1/2 and NF-κB pathways; Methods: Western blot analysis

MTT-based cell viability relative to vehicle-treated controls: MTT after 48 h; 1, 2, 5, 10 and 20 μM. Figure 2A presents mean ± SD. Methods report triplicate evaluation in three independent experiments. — Figure 2A and legend; Methods: Cytotoxicity assays and Statistical analysis

VEGFR2 phosphorylation and downstream ERK1/2 response: Western blots after 48 h at 5, 10 and 20 μM versus 0 μM; phospho and total proteins with β-actin loading control. Representative of three independent experiments. — Figure 5 image and legend; Results: Effects of tivozanib on VEGFR2, AKT, ERK1/2 and NF-κB pathways

In Vivo Studies

In wild-type mice with colonic mucosal wounds, tivozanib treatment was associated with fewer wound-bed blood vessels and more HIF-1α-positive cells at day 4 after injury (both P < 0.01 versus vehicle). The study reported oral gavage at 1 μg/kg once daily. This finding illustrates impaired repair-associated angiogenesis and increased local hypoxia; it is not an antitumor efficacy result. [2]

Impaired angiogenesis and increased hypoxia in injured mouse colon

Animal study · Wild-type mice on a C57BL/6 background with colonic mucosal biopsy wounds [2]

Compared with vehicle controls, tivozanib-treated mice had fewer wound-bed blood vessels and more HIF-1α-positive cells 4 days after mucosal injury. The result links VEGFR inhibition with impaired wound angiogenesis and local hypoxia in this model.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
Blood vessels per wound-bed length	Between-group comparison Decreased; P < 0.01	[2]
HIF-1α-positive cells per wound-bed length	Between-group comparison Increased; P < 0.01	[2]

Conditions shared by the study groups

Route: Oral gavage
Frequency: Once daily
Vehicle: DMSO stock diluted into 300 μL corn oil; final DMSO percentage not specified

Study groups and reported outcomes
Group / dose	Comparator	Observed result	Reference
Tivozanib versus vehicle 1 μg/kg body weight (as printed)	Vehicle-treated mice	At day 4 after injury, fewer wound-bed vessels and more HIF-1α-positive cells; each comparison P < 0.01.	[2]

Tivozanib versus vehicle: Model: Wild-type C57BL/6-background mice with colonic mucosal wounds; general Methods describes adult males and females, 8–16 weeks; Reported limits: Exact treatment start/course and sex distribution for this arm were not specified in consulted text.

Methods and source locations

Compound reported in the paper: Tivozanib; Compound label in the paper: Tivozanib (AV-951)

Model-specific effects of the reported reagent, with the printed dose and missing regimen details preserved.

Figure 4A-F and legend; Results paragraph beginning “To functionally show that hypoxic damage caused muscle necrosis”; Methods: Mice; Inhibitors and compounds (tivozanib paragraph); Statistics

Blood vessels per wound-bed length: CD31 staining; Figure 4E, two-tailed Student’s t test. n = 5 wounds per group from 3 mice per group in 3 experiments; mean ± SEM. — Figure 4A-E and legend; Methods: Statistics

HIF-1α-positive cells per wound-bed length: HIF-1α staining; Figure 4F, Mann-Whitney test. Figure 4A-F uses n = 5 wounds per group from 3 mice per group in 3 experiments; mean ± SEM. — Figure 4A-D,F and legend

Tivozanib versus vehicle · Figure 4A-F and legend; Results paragraph beginning “To functionally show that hypoxic damage caused muscle necrosis”; Methods: Mice; Inhibitors and compounds (tivozanib paragraph); Statistics

Specifications

Manufacturer	Adooq Bioscience
Actions	Inhibitor
CAS Number	475108-18-0
Applications	VEGFR Inhibitor
Formula	C₂₂H₁₉ClN₄O₅
Molecular Weight	454.9
Synonyms	AV-951
SMILES	CC1=CC(=NO1)NC(=O)NC2=C(C=C(C=C2)OC3=C4C=C(C(=CC4=NC=C3)OC)OC)Cl

Storage & Solubility

In Vitro Solubility

Reported Solubility

Solvent	Reported Solubility
DMSO	19 mg/mL (41.76 mM)
Water	Insoluble
Ethanol	Insoluble

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

In Vivo Preparation

Concentration: 1 mg/mL
Vehicle: 2% DMSO+30% PEG 300+ddH2O

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

[1] Momeny M, Sabourinejad Z, Zarrinrad G, et al. Anti-tumour activity of tivozanib, a pan-inhibitor of VEGF receptors, in therapy-resistant ovarian carcinoma cells. Scientific reports (2017). PMID: 28383032 DOI: 10.1038/srep45954 Source material
[2] Manieri NA, Mack MR, Himmelrich MD, et al. Mucosally transplanted mesenchymal stem cells stimulate intestinal healing by promoting angiogenesis. The Journal of clinical investigation (2015). PMID: 26280574 DOI: 10.1172/jci81423 Source material

Publications

7 publications citing this product

Ayaka Kojima, .et al. , Xenobiotica, 2022, Jul;52(7):669-675 PMID: 36251932
Majid Momeny, .et al. , Life Sci, 2021, Dec 15;287:120100 PMID: 34715143
Majid Momeny, .et al. , Eur J Pharmacol, 2020, 882:173298 PMID: 32593665
Majid Momeny, .et al. , Sci Rep, 2017, 7: 45954 PMID: 28383032
Majid Momeny, .et al. , Sci Rep, 2017, 7: 44075 PMID: 28287096
Nicholas A. Manieri, .et al. , J Clin Invest, 2015, Sep 1; 125(9): 3606-3618 PMID: 26280574
Usui T, .et al. , Acta Physiol (Oxf), 2014, 211, 385-394 PMID: 24612679