A Study to Test DSP107 in Combination With Atezolizumab in Comparison With Fruquintinib as a New Treatment for Colorectal Cancer.

The film gives the main points. The full list below is copied from the registry; the study team makes the final decision.

• Age18 Years to no maximum
• SexAll
• Healthy volunteersNo

You may be able to join if

• Are ≥ 18 years of age with a life expectancy of > 3 months.
• Participants with histologically confirmed, inoperable, MSS and/or pMMR CRC which has progressed to, or is intolerant to, specified therapies (and has received prior treatment with no more than 3 lines of therapy).
• Measurable disease per RECIST v1.1.

You cannot join if

• Central nervous system (CNS) metastases unless stable 2 months post definitive therapy with steroids.
• Unresolved AEs of Grade 2 or higher from prior anticancer therapy.
• Past or current history of autoimmune disease or immune deficiency.
• History of other malignancy within 3 years of first study treatment cycle.
• Current or recent treatment with certain therapies including specified anticancer treatments, modulators of CYP3A4 and immunomodulating therapies (prior treatment with CPIs is not exclusory).
• Known allergy or hypersensitivity to any of the test compounds, materials, or contraindication to test product.
• Clinically significant abnormal laboratory safety tests.

This is how the treatment is meant to work. Whether it helps, and how safe it is, is what this trial is testing.

SIRPa-4-1BBL fusion protein DSP107. A bi-functional, trimeric, fusion protein consisting of the extracellular domains (ECDs) of human signal-regulatory protein alpha (SIRPalpha; SIRPa; CD172a) fused to a 4-1BB ligand (4-1BBL), with potential immune checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, the SIRPa-4-1BBL fusion protein DSP107 selectively targets and binds to both CD47 expressed on tumor cells and 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9) expressed on T cells and natural killer (NK) cells. Binding to CD47 blocks the interaction of CD47 with endogenous SIRPa, a cell surface protein expressed on macrophages. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of macrophage activation and phagocytosis of cancer cells. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein-1 (LRP-1), which is expressed on macrophages, and results in macrophage activation and the specific phagocytosis of tumor cells. The binding of 4-1BBL to 4-1BB activates 4-1BB-mediated signaling, induces cytotoxic T-lymphocyte (CTL) proliferation, cytokine production and promotes a CTL-mediated anti-tumor immune response as well as NK-mediated tumor cell killing. The crosslinking specifically enables the activation of 4-1BB-mediated signaling in T-cells and NK cells in the tumor microenvironment (TME), allowing targeted immune responses in the TME. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSC) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, thereby allowing cancer cells to proliferate. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity. NCI Drug Dictionary

atezolizumab. A humanized, Fc optimized, monoclonal antibody directed against the protein ligand PD-L1 (programmed cell death-1 ligand 1; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Atezolizumab binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1; PDCD1) expressed on activated T cells, which may enhance the T-cell-mediated immune response to neoplasms and reverse T-cell inactivation. In addition, by binding to PD-L1, atezolizumab also prevents binding of this ligand to B7.1 (CD80) expressed on activated T cells, which further enhances the T-cell-mediated immune response. PD-L1 is overexpressed on many human cancer cell types and on various tumor-infiltrating immune cells. PD-L1 binding to PD-1 on T cells suppresses the immune system and results in increased immune evasion. PD-1, a transmembrane protein, is a negative regulator of the immune system that limits the expansion and survival of CD8+ T cells. The Fc region of atezolizumab is modified in such a way that it does not induce either antibody-dependent cytotoxicity (ADCC) or complement-dependent cytotoxicity (CDC). NCI Drug Dictionary

fruquintinib. An orally available, small molecule inhibitor of vascular endothelial growth factor receptors (VEGFRs), with potential anti-angiogenic and antineoplastic activities. Upon oral administration, fruquintinib inhibits VEGF-induced phosphorylation of VEGFRs 1, 2, and 3 which may result in the inhibition of migration, proliferation and survival of endothelial cells, microvessel formation, the inhibition of tumor cell proliferation, and tumor cell death. Expression of VEGFRs may be upregulated in a variety of tumor cell types. NCI Drug Dictionary

Treatments listed in the registry

• DSP107 + Atezolizumab (Drug): DSP107 infusion begins ~30 (±10) minutes after completion of atezolizumab infusion on Day 1.
• Fruquintinib (Drug): 5 mg orally, once daily (with or without food), on Days 1-21 of each 28-day cycle, followed by 7 days off.

Randomized · Parallel · masking: None

Main goals

• To determine Median overall survival (mOS) in participants treated with the combination of DSP107 and atezolizumab versus fruquintinib. (From Day 1 until date of death from any cause assessed up to 2 years)

Other goals

• Incidence and severity of adverse events (AEs)
• Changes in 12-lead ECG parameters
• Change in Overall Survival (OS)
• Change from Baseline in Quality of Life (QoL)
• Change from Baseline in Systolic and Diastolic Blood Pressure
• Change from Baseline in Pulse Rate
• To evaluate the immunogenicity of DSP107 when administered in combination with atezolizumab.

Planned enrollment: 90 (estimated).

• University of Colorado Hospital- Anschutz Cancer Center Pavillion (ACP), Aurora, Colorado
• University of Colorado Cancer Center - Highlands Ranch Hospital, Highlands Ranch, Colorado
• Mayo Clinic, Florida City, Florida
• Duke University Medical Center - Duke Cancer Center, Durham, North Carolina
• UPMC Hillman Cancer Center, Pittsburgh, Pennsylvania
• The University of Texas MD Anderson Cancer Center, Texas City, Texas

12 recruiting sites outside the US. Site status as of Oct 30, 2026. Check the live record before contacting a site.

• ClinicalTrials.gov NCT07235293
• NCI Drug Dictionary: C174171
• NCI Drug Dictionary: C106250
• NCI Drug Dictionary: C102852

Registry record reviewed as fetched Oct 30, 2026, last updated by the sponsor Aug 19, 2026. Public record; not medical advice.