BI-1607: An Investigational Bispecific Antibody Targeting VEGF and Angiopoietin-2 for Enhanced Cancer Therapy

I. BI-1607: An Overview of an Investigational Bispecific Antibody

A. Introduction to BI-1607 and its Therapeutic Rationale

BI-1607 is an investigational, engineered antibody currently under development by BioInvent.[1] This therapeutic candidate is distinguished by its design as a platform technology aimed at enhancing the efficacy of, and overcoming resistance to, existing cancer treatments. The primary focus of BI-1607 is to improve outcomes when used in combination with established therapies such as targeted monoclonal antibodies and immune checkpoint inhibitors, addressing the significant clinical challenge of therapeutic resistance in oncology.[1]

The characterization of BI-1607 as a "platform" suggests that its underlying design or dual-targeting mechanism may possess broader applicability. In biopharmaceutical development, a platform technology typically refers to a core molecular design or therapeutic approach that can be adapted for multiple drug candidates or indications. The current investigation of BI-1607 in two distinct oncological settings—melanoma in conjunction with checkpoint inhibitors, and HER2-positive solid tumors in combination with trastuzumab—supports this interpretation.[1] This versatility implies that BioInvent may perceive the dual VEGF/Ang-2 inhibitory strategy, or the specific engineering principles embodied in BI-1607, as a foundational approach. If this strategy proves successful in mitigating treatment resistance and augmenting efficacy in its current trial programs, it is conceivable that its application could be extended to other cancer types where angiogenesis, vascular normalization, and immune modulation are critical determinants of treatment response, or explored with an even wider array of combination partners.

B. Developer: BioInvent

The development of BI-1607 is being conducted by BioInvent, an entity specializing in the discovery and development of novel immunotherapies for cancer.[1]

C. Drug Class: Engineered Bispecific Antibody (Targeting VEGF and Angiopoietin-2)

BI-1607 is classified as an engineered bispecific antibody.[1] The term "bispecific" signifies its capacity to concurrently bind to two distinct molecular targets: Vascular Endothelial Growth Factor A (VEGF-A, commonly referred to as VEGF) and Angiopoietin-2 (Ang-2).[2] This dual-targeting capability is fundamental to its proposed mechanism of action.

The rationale for a bispecific agent targeting both VEGF and Ang-2, rather than combining two separate monospecific antibodies, is strongly supported by preclinical evidence. For instance, in an endotoxin-induced uveitis (EIU) model, which mimics acute ocular inflammation, monotherapies targeting either VEGF or Ang-2 alone were found to be ineffective in ameliorating the condition. In contrast, a bispecific antibody simultaneously neutralizing both VEGF and Ang-2 demonstrated significant therapeutic effects, including a marked reduction in retinal leukocyte infiltration and the number of inflammatory cells in the aqueous humor.[2] This direct comparative evidence underscores that the pathological processes driven by these two factors are likely interconnected to such an extent that inhibiting only one pathway is insufficient to achieve a meaningful therapeutic outcome, at least in the context of this inflammatory model. Consequently, the development of BI-1607 as a bispecific agent appears to be driven by a mechanistic necessity for synergistic or at least potent additive effects that overcome the limitations observed with single-target inhibition.

II. Mechanism of Action and Preclinical Evidence

A. Dual Molecular Targeting: VEGF-A and Angiopoietin-2 (Ang-2)

The therapeutic strategy of BI-1607 is centered on the simultaneous inhibition of two key vascular growth factors, VEGF-A and Angiopoietin-2 (Ang-2). These factors are known to play critical and coordinated roles in the complex processes of pathological angiogenesis (the formation of new blood vessels) and vascular leakage, both of which are hallmarks of tumor growth and progression.[2]

1. Significance of VEGF and Ang-2 in Tumor Angiogenesis, Vascular Permeability, and Inflammation

VEGF-A is a well-characterized protein that acts as a potent mediator of angiogenesis. In the tumor microenvironment, hypoxia (low oxygen levels) frequently triggers the upregulation of VEGF expression.3 VEGF, in turn, stimulates endothelial cell proliferation, migration, and survival, leading to the formation of new blood vessels that supply tumors with nutrients and oxygen. Beyond its role in angiogenesis, VEGF also increases vascular permeability, contributing to fluid leakage from blood vessels, and is recognized as a pro-inflammatory cytokine involved in the chemotaxis (attraction) of macrophages and granulocytes into the tumor site.2

Angiopoietin-2 (Ang-2) is another crucial regulator of vascular biology that often acts in concert with VEGF. Ang-2 is classically considered an antagonist of the Tie2 receptor, thereby counteracting the vessel-stabilizing and anti-inflammatory actions of Angiopoietin-1 (Ang-1).[2] By disrupting vessel stability, Ang-2 can render the vasculature more responsive to angiogenic stimuli like VEGF. Furthermore, Ang-2 promotes vascular permeability, particularly under hypoxic conditions [3], and plays a direct role in inflammation by acting at the leukocyte adhesion step, upregulating the response of endothelial cells to inflammatory signals such as Tumor Necrosis Factor-alpha (TNF-α).[2]

2. Rationale for Synergistic Inhibition

The "coordinate roles" of VEGF and Ang-2 in driving pathological vascular processes suggest that targeting both factors simultaneously may yield a more profound therapeutic effect than inhibiting either one alone.2 General principles in bispecific antibody development support the notion that dual targeting can lead to stronger and more durable effects.4

The interplay between VEGF and Ang-2 is complex. Ang-2 can be viewed as a factor that destabilizes the vasculature and primes it for pathological remodeling, partly by antagonizing the stabilizing effects of Ang-1 via the Tie2 receptor and by enhancing endothelial cell responsiveness to inflammatory cues.[2] Hypoxic tumor environments further exacerbate this by increasing permeability through both VEGF and Ang-2 pathways.[3] In such a destabilized and pro-inflammatory milieu, the potent pro-angiogenic and permeability-enhancing effects of VEGF can be amplified. Therefore, inhibiting Ang-2 may exert direct vessel-stabilizing and anti-inflammatory effects, while also rendering the vasculature less susceptible to VEGF-driven pathology. Concurrently neutralizing VEGF addresses the primary mitogenic and permeability stimulus. This dual blockade strategy aims to disrupt multiple, interdependent steps: reducing the principal angiogenic driver (VEGF) while simultaneously preventing the vessel destabilization and pro-inflammatory priming (Ang-2) that facilitates VEGF's pathological actions. This approach holds the potential for a more comprehensive and durable anti-vascular and anti-inflammatory effect compared to targeting either molecule in isolation.

B. Pharmacological Effects (Observed in Preclinical Models)

Preclinical studies utilizing a bispecific antibody targeting VEGF and Ang-2, serving as a model for BI-1607's mechanism, have provided insights into its potential pharmacological effects.

1. Modulation of the Tumor Microenvironment: Anti-angiogenic and Anti-inflammatory Actions

In the EIU model in mice, systemic administration of an anti-VEGF/Ang-2 bispecific antibody led to a significant decrease in retinal leukocyte infiltration, a reduction in the number of inflammatory cells in the aqueous humor, and a lower protein concentration in the aqueous humor, indicative of reduced vascular leakage.2 While this model represents acute ocular inflammation rather than a tumor setting, these findings are highly relevant to cancer therapy. The ability to reduce leukocyte infiltration and vascular permeability suggests that BI-1607 could modulate the tumor microenvironment by normalizing aberrant tumor vasculature and dampening inflammation, both of which can contribute to tumor progression and resistance to therapy.

2. Impact on NF-κB Signaling Pathway

The same preclinical EIU study demonstrated that treatment with the anti-VEGF/Ang-2 bispecific antibody suppressed the translocation of the NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) p65 subunit into the nucleus and prevented the EIU-induced degradation of IκB-α (inhibitor of kappa B alpha) protein in both retinal and RPE/choroid tissues.2 NF-κB is a critical transcription factor that plays a central role in regulating inflammatory responses, cell survival, and immune cell function. Aberrant NF-κB activation is common in cancer and can promote tumor growth, metastasis, and resistance to therapies. Inhibition of NF-κB signaling by the bispecific antibody points to a specific molecular mechanism underlying its observed anti-inflammatory effects.

The suppression of NF-κB activity may be a key mechanism through which BI-1607 could overcome resistance to immune checkpoint inhibitors (CPIs). Chronic inflammation and persistent NF-κB activation within the tumor microenvironment can foster an immunosuppressive milieu, characterized by T-cell exhaustion or exclusion, thereby limiting the efficacy of CPIs.[1] If BI-1607, by modulating Ang-2's influence on endothelial inflammatory responses and subsequently inhibiting NF-κB, can mitigate these immunosuppressive signals and promote vascular normalization to improve T-cell trafficking, it could "recondition" the tumor microenvironment. Such reconditioning could render tumors more susceptible to the anti-tumor T-cell activity reinvigorated by CPIs, providing a plausible mechanism for synergistic effects.

C. Potential to Overcome Therapeutic Resistance

A primary therapeutic goal for BI-1607 is to enhance the efficacy of existing cancer treatments and overcome mechanisms of therapeutic resistance.[1]

1. Enhancing Efficacy of Existing Cancer Treatments

BI-1607 is conceptualized as a platform technology with the potential to augment the activity of both targeted monoclonal antibodies and immune checkpoint inhibitors.1 This positions it as a combination therapy agent designed to improve upon current standards of care.

2. Preclinical Evidence of Overcoming CTLA-4 Resistance

BioInvent announced proof-of-concept data in 2021 demonstrating the ability of BI-1607 to overcome resistance to CTLA-4 (Cytotoxic T-Lymphocyte Associated Protein 4)-based immunotherapy in preclinical models.1 This finding is particularly significant as CTLA-4 inhibitors, such as ipilimumab, are potent immunotherapies but are associated with considerable immune-related adverse events, and both primary and acquired resistance are common. The ongoing clinical trial in melanoma (NCT06784648) is evaluating BI-1607 in combination with pembrolizumab (an anti-PD-1 antibody) and varying doses of ipilimumab (1 mg/kg and 3 mg/kg).1 This trial design suggests an exploratory strategy to determine if BI-1607 can not only restore or enhance efficacy in settings of CTLA-4 resistance but also potentially allow for the use of lower, and presumably more tolerable, doses of ipilimumab without compromising—or possibly even improving—the anti-tumor response. Achieving comparable or superior efficacy with a reduced toxicity burden would constitute a major clinical advance.

D. Summary of Key Preclinical Studies

The most detailed preclinical study available pertains to an anti-VEGF/Ang-2 bispecific antibody in a model of endotoxin-induced uveitis (EIU) in mice.[2]

1. Efficacy in Ocular Inflammation Models (Endotoxin-Induced Uveitis in mice)

Systemic administration of the anti-VEGF/Ang-2 bispecific antibody resulted in a significant reduction in retinal leukocyte invasion, suppressed NF-κB translocation into the nucleus, and decreased vascular leakage as measured by protein concentration in the aqueous humor. Notably, monotherapies targeting either VEGF or Ang-2 alone did not produce these effects, highlighting the importance of dual inhibition.2 The EIU model, while not a direct cancer model, serves as a robust in vivo system to assess the anti-inflammatory and anti-vascular permeability effects of agents targeting VEGF and Ang-2. The potent effects observed with the bispecific antibody in this model underscore the importance of the anti-inflammatory component of BI-1607's mechanism, which complements its anti-angiogenic properties. This dual action—curtailing aberrant vessel formation and leakage while also dampening local inflammation—is likely crucial for its hypothesized synergistic interactions with immunotherapies, which depend on a tumor microenvironment conducive to immune cell infiltration and function.

III. Clinical Development Program for BI-1607

A. Current Clinical Trial Landscape

BI-1607 is currently being evaluated in early-phase clinical trials across different cancer indications and combination regimens. The following table summarizes the publicly available information on these trials:

Trial ID (if available)	Phase	Indication(s)	Combination Agent(s)	Status	Key Objectives	Snippet Source(s)
NCT06784648	Phase 1b/2a	Unresectable or metastatic melanoma (progressed on anti-PD-1/L1 therapy)	Ipilimumab, Pembrolizumab (KEYTRUDA®)	Enrolling (First patient dosed Dec 2024)	Safety, anti-tumoral activity, dose-finding, pharmacokinetics, immunogenicity	1
Not specified in snippets	Phase 1	HER2+ advanced solid tumors	Trastuzumab	Dose escalation data presented Dec 2023	Safety, tolerability, preliminary efficacy (e.g., stable disease)	1

B. Phase 1b/2a Study in Unresectable or Metastatic Melanoma (NCT06784648)

1. Trial Design and Endpoints

This ongoing study is a Phase 1b/2a clinical trial. The Phase 1b portion is designed to determine the recommended doses of BI-1607 when used in combination, while the Phase 2a portion will assess the treatment's effectiveness in inducing tumor shrinkage.5 The study incorporates four distinct cohorts, which will evaluate two different dose levels of BI-1607 in combination with two different dose levels of the CTLA-4 antibody ipilimumab (3 mg/kg, the approved dose for melanoma, and a lower dose of 1 mg/kg). All cohorts will also receive a standard 200 mg flat dose of pembrolizumab.1 The primary objectives include assessing the safety and tolerability of the combination and determining the recommended Phase 2 dose (RP2D). Secondary objectives include evaluating preliminary anti-tumor activity.5

2. Investigational Combination: BI-1607 with Pembrolizumab and Ipilimumab

The trial investigates BI-1607 in combination with pembrolizumab (KEYTRUDA®, an anti-PD-1 antibody) and ipilimumab (YERVOY®, an anti-CTLA-4 antibody).1 KEYTRUDA® is a registered trademark of Merck Sharp & Dohme LLC, a subsidiary of Merck & Co., Inc., Rahway, NJ, USA.1 This triplet immunotherapy combination aims to simultaneously target multiple immune checkpoint pathways (PD-1 and CTLA-4) while concurrently modulating the tumor microenvironment through BI-1607's dual inhibition of VEGF and Ang-2. The rationale is to achieve enhanced T-cell activation and anti-tumor immunity, with BI-1607 potentially improving the efficacy of the dual checkpoint blockade and overcoming resistance mechanisms.

3. Patient Population and Current Enrollment Status

The study is enrolling adult patients (≥ 18 years) with histologically confirmed unresectable or metastatic melanoma whose disease has progressed following prior treatment with an anti-PD-1 or anti-PD-L1 monoclonal antibody.5 Eligible patients must have an ECOG performance status of 0 or 1 and a life expectancy of at least 12 weeks.5 The first patient was enrolled in this trial in December 2024.1 The study is actively recruiting, with an estimated enrollment of 35 participants, at sites including the Sarah Cannon Research Institute UK.6

C. Phase 1 Study in HER2+ Advanced Solid Tumors

1. Trial Design and Endpoints

This was a Phase 1 dose-escalation study, a standard design for first-in-human trials aimed at establishing the safety, tolerability, and maximum tolerated dose (MTD) of a new investigational agent or combination.1

2. Investigational Combination: BI-1607 with Trastuzumab

In this study, BI-1607 was evaluated in combination with trastuzumab, an anti-HER2 monoclonal antibody.1 This investigation in HER2-positive tumors with trastuzumab expands BI-1607's potential application beyond melanoma and assesses its synergy with a different class of targeted therapy. This aligns with the "platform" concept for BI-1607, suggesting its utility across various oncologic settings. The combination with trastuzumab implies that BI-1607’s microenvironment-modulating effects might enhance trastuzumab's activity. Trastuzumab's mechanisms of action include inhibiting HER2 signaling and inducing antibody-dependent cell-mediated cytotoxicity (ADCC). By normalizing tumor vasculature, BI-1607 could potentially improve the delivery of trastuzumab to tumor cells and facilitate the infiltration of immune effector cells, such as Natural Killer (NK) cells, which are crucial for ADCC. Furthermore, by mitigating Ang-2-mediated inflammation and potentially modulating NF-κB activity, BI-1607 might foster a tumor microenvironment more supportive of effector immune cell function, thereby potentially overcoming resistance mechanisms that can limit trastuzumab's efficacy.

IV. Emerging Clinical Data: Safety and Preliminary Efficacy

A. Safety and Tolerability Profile

1. Findings from the Phase 1 study in HER2+ Solid Tumors

Initial clinical data from the Phase 1 dose-escalation study of BI-1607 in combination with trastuzumab in subjects with HER2+ advanced solid tumors were presented in December 2023. These data indicated that the combination treatment was well tolerated. Importantly, no serious adverse events (SAEs) deemed related to BI-1607 were observed in this early trial.1 A favorable safety profile is a critical early indicator, particularly for agents intended for use in combination regimens.

2. Expected Safety Assessments in Ongoing Melanoma Trial

The ongoing Phase 1b/2a melanoma trial (NCT06784648) has safety and tolerability as primary objectives. Participants will undergo regular monitoring of their health status, including vital signs, laboratory tests, and electrocardiograms (ECGs), with close tracking of any adverse events.5 A key aspect of this trial will be to delineate the safety profile of the BI-1607, pembrolizumab, and ipilimumab triplet. Dual checkpoint inhibition with anti-PD-1 and anti-CTLA-4 agents is associated with a higher incidence and severity of immune-related adverse events (irAEs) compared to anti-PD-1 monotherapy. The addition of BI-1607, which has immunomodulatory potential via VEGF/Ang-2 inhibition and NF-κB pathway effects, will be carefully monitored to ascertain whether it exacerbates these irAEs. Conversely, if BI-1607 enables effective anti-tumor activity at lower, potentially less toxic doses of ipilimumab (as is being explored in the trial's cohort design 1), it could lead to an improved therapeutic index for the combination.

B. Preliminary Anti-Tumor Activity and Efficacy Signals

1. Observations in HER2+ Solid Tumors

In the Phase 1 study of BI-1607 combined with trastuzumab in patients with HER2+ advanced solid tumors, stable disease (SD) was observed in 6 out of 11 evaluable patients.1 In the context of a Phase 1 trial involving patients with advanced, likely heavily pre-treated cancers, achieving stable disease can be an encouraging early sign of biological activity, suggesting that the treatment is exerting some measure of control over tumor growth.

2. Efficacy Endpoints in Melanoma Trial

The Phase 2a portion of the melanoma trial (NCT06784648) is designed to assess the anti-tumor activity of the BI-1607 combination.5 Efficacy objectives include determining the proportion of patients whose tumors shrink (objective response rate) and the duration of such responses.6

The following table summarizes the preliminary safety and efficacy data available for BI-1607:

Study / Indication	Combination Agent(s)	Key Safety Findings (BI-1607 Related)	Key Efficacy Findings	Snippet Source(s)
Phase 1 / HER2+ Adv. Solid Tumors	Trastuzumab	Well tolerated, No BI-1607 related SAEs	Stable Disease in 6/11 evaluable pts	1
Phase 1b/2a / Adv. Melanoma	Ipilimumab, Pembrolizumab	Data pending (trial ongoing)	Data pending (trial ongoing)	1
Preclinical / EIU Model	Bispecific Ab (VEGF/Ang-2) alone	Not applicable (animal model)	Reduced inflammation & leakage	2

C. Pharmacokinetics and Immunogenicity

The melanoma trial (NCT06784648) will also evaluate the pharmacokinetic (PK) profile of BI-1607 (how the drug is absorbed, distributed, metabolized, and excreted by the body) and its immunogenicity (the propensity to elicit an immune response against the drug itself, potentially forming anti-drug antibodies).[6] These are standard and crucial assessments for all biologic drug candidates, as PK data informs optimal dosing strategies, and immunogenicity can impact both the safety and efficacy of the therapeutic.

V. Expert Analysis and Future Outlook

A. Therapeutic Potential and Position in Oncology Landscape

BI-1607 represents a rationally designed therapeutic agent employing a dual VEGF/Ang-2 inhibition strategy. This approach aims to modulate the tumor microenvironment in ways that may overcome resistance to established therapies, including immune checkpoint inhibitors and targeted antibodies. The strategy of simultaneously targeting VEGF and Ang-2 with BI-1607 seeks to provide a more comprehensive blockade of pathological tumor vascularization and associated inflammation compared to agents that inhibit only the VEGF pathway. Resistance to therapies targeting solely the VEGF pathway is a common clinical challenge. Angiopoietin-2 has been implicated not only in promoting angiogenesis and vascular destabilization but also in fostering an inflammatory and immunosuppressive tumor microenvironment, which can contribute to therapeutic resistance. By neutralizing both VEGF and Ang-2, BI-1607 may therefore offer advantages in overcoming these resistance mechanisms, achieving more profound vascular normalization, and creating a tumor microenvironment more amenable to the actions of immunotherapies. This broader mechanistic impact, particularly the anti-inflammatory effects potentially mediated via NF-κB inhibition as suggested by preclinical models [2], could lead to improved efficacy and synergistic effects when combined with checkpoint inhibitors or other targeted agents. If validated in ongoing and future clinical trials, BI-1607 could address significant unmet medical needs for patients whose cancers have become refractory to current treatment modalities.

B. Key Development Milestones and Future Research Directions

Critical upcoming milestones for the BI-1607 program include the initial safety and efficacy readouts from the Phase 1b/2a melanoma trial (NCT06784648), particularly the determination of the recommended Phase 2 dose for the triplet combination and preliminary objective response rates in this PD-1/L1 refractory population. Future research directions will likely involve the development of predictive biomarkers to identify patient populations most likely to benefit from BI-1607-containing regimens. Given its mechanism of action targeting VEGF, Ang-2, and influencing the NF-κB pathway, potential biomarkers could include baseline tumor expression levels of VEGF and Ang-2, characteristics of the tumor vasculature (e.g., vessel maturity, pericyte coverage), the extent and nature of the inflammatory infiltrate, or the activation status of the NF-κB pathway within tumor or immune cells. The development of such biomarkers would enable patient selection strategies in later-phase trials, increasing the likelihood of demonstrating clinical benefit and ultimately facilitating a more personalized therapeutic approach. Furthermore, based on its conceptualization as a "platform" technology [1], positive results in current trials could spur exploration in other tumor types or with different combination partners.

C. Comparative Context: Other Dual VEGF/Ang-2 Inhibitors

The concept of dual VEGF/Ang-2 inhibition is gaining traction in therapeutic development. Faricimab (Vabysmo), a bispecific antibody targeting both VEGF-A and Ang-2, has achieved regulatory approval and demonstrated superior disease control compared to anti-VEGF monotherapies in ophthalmic conditions such as neovascular age-related macular degeneration (nAMD) and diabetic macular edema (DME).7 While ophthalmology and oncology are distinct therapeutic areas, the fundamental roles of VEGF and Ang-2 in regulating vascular permeability, inflammation, and neovascularization share underlying biological commonalities. The clinical validation of dual VEGF/Ang-2 inhibition by Faricimab in eye diseases lends strong support to the biological rationale for this strategy.

In the oncology space, other investigational agents targeting both pathways are also emerging. For example, an Ang-2-VEGF-A CrossMab, a novel bispecific human IgG1 antibody, has demonstrated potent antitumor, antiangiogenic, and antimetastatic efficacy in various preclinical tumor models.4 The development of such agents indicates a growing interest in this dual-targeting approach, positioning BI-1607 within an innovative class of therapeutics. The specific molecular engineering, pharmacokinetic profile, and chosen combination strategies of BI-1607 will be critical factors in differentiating it from other agents pursuing similar dual targets.

D. Concluding Remarks

BI-1607 is an investigational bispecific antibody with a compelling, rationally designed mechanism of action focused on dual inhibition of VEGF and Ang-2. This strategy holds promise for modulating the tumor microenvironment to enhance the efficacy of, and overcome resistance to, existing cancer therapies, particularly immune checkpoint inhibitors and targeted antibodies. Early preclinical and limited Phase 1 clinical data are encouraging, suggesting anti-inflammatory effects, anti-vascular permeability, and a tolerable safety profile in combination with trastuzumab, with initial signs of anti-tumor activity (stable disease).[1]

The ongoing Phase 1b/2a trial in advanced melanoma (NCT06784648), combining BI-1607 with dual checkpoint blockade (pembrolizumab and ipilimumab), is a critical study. Close attention should be paid to its forthcoming results, particularly regarding the safety of this triplet combination and its efficacy in a challenging PD-1/L1 refractory patient population. The trial's exploration of different ipilimumab doses in combination with BI-1607 is a noteworthy design feature that may shed light on strategies to optimize the benefit/risk profile of CTLA-4 blockade.[1] The "platform" nature of BI-1607 also suggests potential for broader applications should current trials yield positive outcomes. Continued monitoring of clinical trial data, presentations at scientific conferences, and publications will be essential to fully assess the therapeutic potential of BI-1607 in the evolving landscape of cancer treatment.

Works cited

1. BI-1607 - BioInvent International, accessed June 9, 2025, https://www.bioinvent.com/en/clinical-programs/our-programs/bi-1607
2. Anti -VEGF/Ang2 bi-specific antibody ameliorates endotoxin-induced uveitis in mice | IOVS, accessed June 9, 2025, https://iovs.arvojournals.org/article.aspx?articleid=2267690
3. Blood vessel maturation, vascular phenotype and angiogenic potential in malignant melanoma - PubMed Central, accessed June 9, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC5528279/
4. Bispecific Antibodies Targeting VEGF and ANG2 - Creative Biolabs, accessed June 9, 2025, https://www.creative-biolabs.com/bsab/bispecific-antibodies-targeting-vegf-and-ang2.htm
5. Study of BI-1607, Ipilimumab, and Pembrolizumab for Patients with Advanced Melanoma, accessed June 9, 2025, https://clinicaltrials.eu/trial/study-of-bi-1607-ipilimumab-and-pembrolizumab-for-patients-with-advanced-melanoma/
6. Different Doses of BI-1607 in Combination with Pembrolizumab and Ipilimumab, in Participants with Unresectable or Metastatic Melanoma - National Brain Tumor Society, accessed June 9, 2025, https://trials.braintumor.org/trials/NCT06784648
7. Applications of Bispecific Antibodies in Therapeutics - Biointron, accessed June 9, 2025, https://www.biointron.com/blog/applications-of-bispecific-antibodies-in-therapeutics.html