Sporos Bioventures Diversified Pipeline
Novel and Validated Targets with Clear Responder Hypothesis
IN VIRTO DISCOVERY
IN VIVO PRECLINICAL
POC IND
ENABLING PHASE I
PROGRAM
SPR1
Precision Oncology
PHASE
IND Enabling
PROGRAM
SPR1
Precision Oncology
PHASE
IND Enabling
Target: TEAD
Focus: Cancers with Hippo-driver mutations / aberrations and YAP/TAZ hyperactivation
TARGET
TEAD
FOCUS
Cancers with Hippo-driver mutations / aberrations and YAP/TAZ hyperactivation
SPR1 is a novel small molecule, isoform-selective inhibitor of TEAD1 / TEAD4. SPR1 targets cancers driven by mutations in the Hippo pathway, a key regulator of cell proliferation and oncogenesis not yet extensively targeted in precision oncology. The YAP1/TAZ co-activators and the TEAD family of transcription factors, which consists of four paralogs (TEAD1-4), execute the pro-cancerous effects of the Hippo pathway through transcription of pro-proliferative and anti-apoptotic genes. Hippo pathway activation has also emerged as a key mechanism of resistance to inhibitors of the MAPK pathway, making TEAD inhibitors a prime candidate for combination therapy with therapeutics targeting the MAPK pathway.
PROGRAM
SPR4
Precision Oncology
PHASE
Discovery in Vitro
PROGRAM
SPR4
Precision Oncology
PHASE
Discovery in Vitro
Target: Undisclosed
Focus: PTEN-deficient cancers
TARGET
Undisclosed
FOCUS
PTEN-deficient cancers
SPR4 is a small molecule targeting PTEN-deficient cancers. Genetic deletions of PTEN are mutually exclusive in human tumors and simultaneous genetic deletions of PTEN prevents PTEN-null tumorigenesis. Our undisclosed target for PTEN-deficient cancers plays a role in reversing immunosuppression and may synergize with immune checkpoint inhibitors.
PROGRAM
ASY-87
Precision Oncology
PHASE
Discovery in Vitro
PROGRAM
ASY-87
Precision Oncology
PHASE
Discovery in Vitro
Target: Cell-surface heat shock protein 70 (HSP70)
Focus: T-cell lymphomas, triple-negative breast cancer, myeloma
TARGET
Cell-surface heat shock protein 70 (HSP70)
FOCUS
T-cell lymphomas, triple-negative breast cancer, myeloma
ASY-87 is an antibody drug conjugate (ADC) that binds to the cell-surface form of HSP70 and carries a toxic payload to the cancer cell. The cell-surface form of HSP70 is differentially expressed and increased on cancer cells as compared to healthy cells. HSP70’s role is especially crucial in shuttling tumor-derived (or autoreactive or viral) antigens to dendritic cells (DCs), which capture, process, and present tumor antigens to other immune cells to initiate the development of immune responses against all cancers.
PROGRAM
ASY-77A
Tumor Biology / TME
PHASE
IND Enabling
PROGRAM
ASY-77A
Tumor Biology / TME
PHASE
IND Enabling
Target: Extracellular heat shock protein 70 (HSP70)
Focus: Triple-negative breast cancer, Multiple Myeloma
TARGET
Extracellular heat shock protein 70 (HSP70)
FOCUS
Triple-negative breast cancer, Multiple Myeloma
ASY-77A is an antibody that enhances antigen presentation by targeting the extracellular form of heat shock protein (HSP70), a molecule central to antigen delivery to the immune system. HSP70’s role is especially crucial in shuttling tumor-derived (or autoreactive or viral) antigens to dendritic cells (DCs), which capture, process, and present tumor antigens to other immune cells to initiate the development of immune responses against all cancers.
PROGRAM
SPR2
Tumor Biology / TME
PHASE
Discovery in Vitro
PROGRAM
SPR2
Tumor Biology / TME
PHASE
Discovery in Vitro
Target: CXCR2
Focus: Cancers resistant to immunotherapy
TARGET
CXCR2
FOCUS
Cancers resistant to immunotherapy
SPR2 is a small molecule inhibitor of CXCR2, which prevents recruitment of myeloid-derived suppressor cells (MDSCs) thereby removing impediments of checkpoint blockade immuno-therapies. MDSCs are critical negative regulators of anti-tumor immune response and tumors with high levels of infiltration by MDSCs have been associated with poor patient outcome and resistance to therapies.
PROGRAM
SPR3
Tumor Biology / TME
PHASE
Discovery in Vitro
PROGRAM
SPR3
Tumor Biology / TME
PHASE
Discovery in Vitro
Target: CCR2
Focus: Cancers resistant to MAPK inhibition and / or to immunotherapy
TARGET
CCR2
FOCUS
Cancers resistant to MAPK inhibition and / or to immunotherapy
SPR3 is a small molecule inhibitor of CCR2, a druggable chemokine receptor that forms lynchpin in a signaling cascade that allows KRAS inhibition bypass through recruitment of MDSCs. CCR2 is a major signaling node for the conversion of neutrophils into anti-tumor immuno-suppressive MDSCs.