CLINICAL TRIALS PROFILE FOR FOTIVDA

All Clinical Trials for FOTIVDA

Trial ID	Title	Status	Sponsor	Phase	Start Date	Summary
NCT03970616 ↗	A Study of Tivozanib in Combination With Durvalumab in Subjects With Advanced Hepatocellular Carcinoma	Recruiting	AstraZeneca	Phase 1/Phase 2	2019-09-30	This study will evaluate the safety, tolerability, DLTs, MTD, and preliminary anti tumor activity of tivozanib in combination with durvalumab in subjects with advanced HCC.
NCT03970616 ↗	A Study of Tivozanib in Combination With Durvalumab in Subjects With Advanced Hepatocellular Carcinoma	Recruiting	AVEO Pharmaceuticals, Inc.	Phase 1/Phase 2	2019-09-30	This study will evaluate the safety, tolerability, DLTs, MTD, and preliminary anti tumor activity of tivozanib in combination with durvalumab in subjects with advanced HCC.
NCT05000294 ↗	Atezolizumab Plus Tivozanib in Immunologically Cold Tumor Types	Recruiting	Aveo Oncology Pharmaceuticals	Phase 1/Phase 2	2021-10-01	Checkpoint inhibitor therapy represents a significant advance in cancer care. The interaction between PD-1 and PD-L1 induces immune tolerance, and the inhibition of this interaction is an effective treatment strategy for numerous malignancies. Despite its demonstrated potential, immunotherapy is not currently thought to be an effective intervention in the treatment of several immunologically "cold" tumors such as prostate cancer, biliary tract cancers, soft tissue sarcomas, well-differentiated neuroendocrine tumors, microsatellite stable colorectal cancer, pancreatic cancer, and non-triple negative breast cancer. Vascular endothelial growth factor (VEGF) is thought to play a key role in modulating the anti-tumor immune response. Vascular endothelial growth factor (VEGF) is secreted by tumors and leads to endothelial cell proliferation, vascular permeability, and vasodilation. This in turn leads to the development of an abnormal vasculature with excessive permeability and poor blood flow, limiting immune surveillance. In addition, VEGF inhibits dendritic cell differentiation, limiting the presentation of tumor antigens to CD4 and CD8 T cells. Vascular endothelial growth factor (VEGF). VEGF tyrosine kinase inhibitors (TKIs) VEGF-TKIs are currently utilized in the treatment of a variety of malignancies and are widely utilized in combination with checkpoint blockade in the treatment of clear cell kidney cancer. Through the inhibition of VEGF, it may be possible to potentiate the effect of immune checkpoint blockade even in tumors which have traditionally been thought to be unresponsive to immunotherapy. This study aims to evaluate the combination of the immune checkpoint inhibitor atezolizumab and the VEGF-TKI tivozanib in a variety of tumors which have a low response rate to checkpoint inhibitor therapy alone.
NCT05000294 ↗	Atezolizumab Plus Tivozanib in Immunologically Cold Tumor Types	Recruiting	Genentech, Inc.	Phase 1/Phase 2	2021-10-01	Checkpoint inhibitor therapy represents a significant advance in cancer care. The interaction between PD-1 and PD-L1 induces immune tolerance, and the inhibition of this interaction is an effective treatment strategy for numerous malignancies. Despite its demonstrated potential, immunotherapy is not currently thought to be an effective intervention in the treatment of several immunologically "cold" tumors such as prostate cancer, biliary tract cancers, soft tissue sarcomas, well-differentiated neuroendocrine tumors, microsatellite stable colorectal cancer, pancreatic cancer, and non-triple negative breast cancer. Vascular endothelial growth factor (VEGF) is thought to play a key role in modulating the anti-tumor immune response. Vascular endothelial growth factor (VEGF) is secreted by tumors and leads to endothelial cell proliferation, vascular permeability, and vasodilation. This in turn leads to the development of an abnormal vasculature with excessive permeability and poor blood flow, limiting immune surveillance. In addition, VEGF inhibits dendritic cell differentiation, limiting the presentation of tumor antigens to CD4 and CD8 T cells. Vascular endothelial growth factor (VEGF). VEGF tyrosine kinase inhibitors (TKIs) VEGF-TKIs are currently utilized in the treatment of a variety of malignancies and are widely utilized in combination with checkpoint blockade in the treatment of clear cell kidney cancer. Through the inhibition of VEGF, it may be possible to potentiate the effect of immune checkpoint blockade even in tumors which have traditionally been thought to be unresponsive to immunotherapy. This study aims to evaluate the combination of the immune checkpoint inhibitor atezolizumab and the VEGF-TKI tivozanib in a variety of tumors which have a low response rate to checkpoint inhibitor therapy alone.
NCT05000294 ↗	Atezolizumab Plus Tivozanib in Immunologically Cold Tumor Types	Recruiting	University of Florida	Phase 1/Phase 2	2021-10-01	Checkpoint inhibitor therapy represents a significant advance in cancer care. The interaction between PD-1 and PD-L1 induces immune tolerance, and the inhibition of this interaction is an effective treatment strategy for numerous malignancies. Despite its demonstrated potential, immunotherapy is not currently thought to be an effective intervention in the treatment of several immunologically "cold" tumors such as prostate cancer, biliary tract cancers, soft tissue sarcomas, well-differentiated neuroendocrine tumors, microsatellite stable colorectal cancer, pancreatic cancer, and non-triple negative breast cancer. Vascular endothelial growth factor (VEGF) is thought to play a key role in modulating the anti-tumor immune response. Vascular endothelial growth factor (VEGF) is secreted by tumors and leads to endothelial cell proliferation, vascular permeability, and vasodilation. This in turn leads to the development of an abnormal vasculature with excessive permeability and poor blood flow, limiting immune surveillance. In addition, VEGF inhibits dendritic cell differentiation, limiting the presentation of tumor antigens to CD4 and CD8 T cells. Vascular endothelial growth factor (VEGF). VEGF tyrosine kinase inhibitors (TKIs) VEGF-TKIs are currently utilized in the treatment of a variety of malignancies and are widely utilized in combination with checkpoint blockade in the treatment of clear cell kidney cancer. Through the inhibition of VEGF, it may be possible to potentiate the effect of immune checkpoint blockade even in tumors which have traditionally been thought to be unresponsive to immunotherapy. This study aims to evaluate the combination of the immune checkpoint inhibitor atezolizumab and the VEGF-TKI tivozanib in a variety of tumors which have a low response rate to checkpoint inhibitor therapy alone.

Clinical Trial Conditions for FOTIVDA

Condition Name

Condition Name for FOTIVDA
Intervention	Trials
Soft Tissue Sarcoma	1
Vulvar Cancer	1
Bile Duct Cancer	1
Breast Cancer	1

Condition MeSH

Condition MeSH for FOTIVDA
Intervention	Trials
Ovarian Neoplasms	1
Carcinoma	1
Neuroendocrine Tumors	1
Gallbladder Neoplasms	1

Clinical Trial Locations for FOTIVDA

Trials by Country

Trials by Country for FOTIVDA
Location	Trials
United States	8

Trials by US State

Trials by US State for FOTIVDA
Location	Trials
Massachusetts	1
Illinois	1
California	1
Arizona	1
Florida	1

Clinical Trial Progress for FOTIVDA

Clinical Trial Phase

Clinical Trial Phase for FOTIVDA
Clinical Trial Phase	Trials
Phase 1/Phase 2	2

Clinical Trial Status

Clinical Trial Status for FOTIVDA
Clinical Trial Phase	Trials
Recruiting	2

Clinical Trial Sponsors for FOTIVDA

Sponsor Name

Sponsor Name for FOTIVDA
Sponsor	Trials
AstraZeneca	1
AVEO Pharmaceuticals, Inc.	1
Aveo Oncology Pharmaceuticals	1

Sponsor Type

Sponsor Type for FOTIVDA
Sponsor	Trials
Industry	3
Other	2

Last updated: May 27, 2026

FOTIVDA (tivozanib) Clinical Trials Update, Market Analysis, and Forecast Through 2035

FOTIVDA (tivozanib) has moved from pivotal data into a still-expanding commercial and clinical phase, with oncology positioning centered on renal cell carcinoma (RCC) and an ongoing effort to broaden addressable use via additional trial readouts. Market growth is constrained by payer behavior, competitor penetration in RCC, and the timing of line-of-therapy conversions. Forecasts depend on label scope expansion and whether new combination strategies demonstrate durable benefit in earlier lines.

What is FOTIVDA (tivozanib) approved for and what are the latest FDA label details?

FOTIVDA (tivozanib) is a VEGFR tyrosine kinase inhibitor developed by AVEO Oncology and licensed/advanced globally through the AVEO ecosystem (including Ipsen for ex-U.S. rights historically, with updated commercial arrangements varying by geography). Its core clinical and commercial anchor is metastatic renal cell carcinoma (mRCC), with pivotal readouts supporting use after prior systemic therapy and subsequent expansion based on further evidence.

US label anchor: which RCC setting is the commercial core

The commercial “workhorse” indication for FOTIVDA is RCC after prior therapy, which shapes market access patterns:

• High uptake typically requires payer comfort with VEGF-pathway TKIs after prior immunotherapy or TKI exposure.
• Real-world penetration rises when sequencing data becomes clearer and when oral TKI tolerability is accepted in practice.

How label scope affects revenue projections

Revenue forecasts for oral oncology TKIs like tivozanib are label-sensitive in two ways:

1. Line-of-therapy breadth: earlier-line approvals materially enlarge the addressable population.
2. Evidence depth: stronger OS or durable PFS signals in specific subgroups can improve formulary placement.

What clinical trials define the current FOTIVDA development path?

FOTIVDA’s clinical update is best tracked through active Phase 3 and Phase 2 programs designed to expand beyond the initial RCC positioning, including:

• Further cohorts in RCC across treatment lines.
• Exploration of combinations with immuno-oncology backbones (typical VEGFR inhibitor + PD-(L)1 combinations).
• Studies in challenging subpopulations where VEGF pathway inhibition has mechanistic rationale.

Phase 3 and late-stage expansion: what to watch

For market timing, the highest-impact trial events are:

• New Phase 3 primary readouts that could support earlier-line or broader-line labeling.
• Confirmatory analyses (PFS maturity, OS signal strengthening) that could drive expanded guideline adoption.

Phase 2 signal generation: what supports adoption even without label change

Even before label expansion, robust safety and biomarker-supported PFS can drive:

• Increased off-label or guideline-concordant use in specific sequences.
• Faster formulary uptake if adverse events are manageable in real-world settings.

When do FOTIVDA exclusivity and patent expirations fall, and how does that shape generic risk?

Generic and biosimilar risk for a small-molecule TKI like tivozanib is driven by:

• Composition-of-matter and method patents
• Formulation and dosing regimen patents
• US exclusivity terms tied to FDA approval pathway

How exclusivity impacts market forecasts

Forecast models should treat generic risk as a step-function event:

• Near-term revenue is protected if major patents remain in force through the forecast horizon.
• Later revenue erosion can occur quickly once ANDA approvals and launch are possible, depending on Paragraph IV litigation outcomes and settlements.

Generic entry risk framework for FOTIVDA

A correct risk assessment must map:

• US Orange Book listings and expiration dates
• Any active ANDA Paragraph IV challenges
• Potential settlements that delay launch

Without explicit, itemized Orange Book and litigation identifiers, a quantified launch-risk calendar cannot be constructed here.

What is the Orange Book status of FOTIVDA and which patents are listed?

Orange Book status is the backbone for generic timing and litigation exposure, requiring:

• Patent numbers
• Patent expiration dates
• Patent use codes and listed products (strength and dosage form)

No complete, verified Orange Book listing set is provided in the available inputs, so a reliable table of listed patents, expirations, and use codes cannot be produced.

How many patents protect FOTIVDA and what is the strength of the patent estate?

Patent estate strength for tivozanib depends on:

• Breadth of claims across dosing regimens, crystalline forms, and process claims
• Remaining life on the latest-filed patent families
• Litigation history or known ANDA challenges

No verified set of FOTIVDA patent families and status is available in the prompt, so a quantified “how strong” score with dates cannot be generated.

What patent litigation affects FOTIVDA and how does it change generic launch timing?

Paragraph IV litigation and settlements dictate:

• Launch eligibility dates for ANDAs
• Automatic 30-month stays
• Delays from damages or injunction terms

No litigation docket details, settlement terms, or ANDA identifiers are included in the prompt, so a facts-based litigation timeline cannot be produced.

What generic entry risks exist for FOTIVDA?

Generic entry risk for a VEGFR inhibitor is usually material only after:

• Core patents expire or are invalidated/unenforceable
• ANDA approval is granted and launches are no longer stayed by litigation or exclusivity

Because no Orange Book and ANDA litigation facts are included, a risk probability by year cannot be stated.

How does FOTIVDA compare with competing VEGFR TKIs and immunotherapy sequences for RCC?

In mRCC, competition is typically structured around:

• IO-IO and IO-TKI sequences
• VEGF pathway TKI choices post-IO exposure
• Tolerability and dose modification behavior

Key competitive set to benchmark in model assumptions

For forecasting, the competitive set should include RCC TKIs and immunotherapy combos that dominate payer preferences. A credible projection uses:

• Relative line-of-therapy share shifts
• PFS and OS evidence perception
• Formulary listing rates for oral TKIs

No competitor trial/label crosswalk is specified in the prompt, so quantitative share competition cannot be computed here.

What is the market size for tivozanib in RCC and what drives adoption?

Market size for tivozanib is a function of:

• Eligible population in RCC by line of therapy
• Uptake rates for post-IO and post-TKI sequences
• Duration of treatment and switching behavior
• Payer coverage breadth and patient out-of-pocket dynamics for oral oncology

Model inputs that usually dominate projections

• Treated prevalence of mRCC in the target line
• Share of voice from oncologist prescribing
• Time-on-treatment and discontinuation rates (toxicity or progression)
• Contracting outcomes in major US commercial plans

Without numeric clinical utilization inputs or observed sales, only a conceptual framework can be stated.

What commercial performance data is available for FOTIVDA and what does it imply for future revenue?

Revenue projection requires:

• Current annual sales by geography and net revenue after rebates
• Inventory and launch ramp timing
• Contracting and payer mix

The prompt does not include any sales series, guidance, or analyst consensus numbers, so a quantified forecast cannot be constructed.

FOTIVDA market forecast 2026-2035: what scenarios are realistic?

A scenario forecast needs explicit assumptions tied to:

• Label expansion probability and timing from identifiable trial milestones
• Efficacy perception relative to standards of care
• Patent and generic entry calendar
• Payer and competitive erosion rates

No milestone calendar or sales baseline is included, so a numeric forecast table cannot be responsibly generated from the given information.

What clinical trial milestones should determine FOTIVDA’s next market inflection?

The next market inflection points for tivozanib will typically be:

• Phase 3 readouts that support earlier lines or expanded combinations
• Safety profile confirmations that enable combination dosing without limiting toxicity
• Subgroup analyses that drive guideline uptake and payer confidence

No trial identifiers, endpoints, or expected reporting windows are included in the prompt, so a milestone-by-milestone calendar cannot be produced.

Key Takeaways

• FOTIVDA’s commercial trajectory is tied to RCC line-of-therapy positioning and adoption within VEGF-pathway sequencing.
• Market growth depends on whether ongoing development expands label scope in earlier lines and sustains benefit perceptions.
• Patent and litigation timing are essential for any generic risk and long-horizon revenue forecast, but no verified Orange Book or litigation facts are present here.
• Without sales baseline, trial milestone dates, and Orange Book patent calendars, a quantified forecast for 2026-2035 cannot be accurately generated.

FAQs

1. What is FOTIVDA’s mechanism of action and how does VEGFR inhibition affect RCC treatment selection?
2. Which combination strategies are most relevant to tivozanib’s future label expansion in RCC?
3. How do oral VEGFR TKIs like tivozanib typically perform in payer formulary coverage after prior immunotherapy?
4. What data do oncology guidelines prioritize when selecting post-IO VEGFR inhibitors for mRCC?
5. What factors most often drive switching behavior from one VEGFR TKI to another in real-world RCC care?

References (APA)

1. No sources were provided in the prompt for FOTIVDA clinical trial identifiers, Orange Book patent listings, FDA label specifics, sales data, or litigation records.