CD47 (CD47 Molecule)

Macrophages are thus a double-edged sword, inhibiting the development of metastatic disease by phagocytosing disseminated melanoma cells, but promoting the emergence of a hyper-metastatic subpopulation of cells in inflamed regions of primary tumors as a consequence of sustained interferon production. Sustained interferon exposure within inflamed regions of primary tumors dramatically increases the metastatic potential of a subpopulation of melanoma cells, partly by promoting CD47 expression, which protects against phagocytosis by macrophages.

Moreover, CYN-CDA@Alb also avoids the usually increased innate and adaptive immune resistance after radiotherapy by depressing CD47 and PD-L1. Our findings altogether suggest the potential usage of copper ion-depleting nanoparticles as substitutes for CD47/PD-L1 bispecific antibodies to simultaneously overcome innate and adaptive immune-resistance.

Stromal myeloid cells showed increased CD47 and PD-1 expression. Our study identified distinct epigenetic profiles in sacral chordomas, which were associated with recurrence, and revealed expression of checkpoint markers TIM3, CD47 and PD-1, warranting further investigation through functional validation.

We present multi-factor models that predict second recurrence and prognosis in recurrent HCC. This prognostic tool can inform personalized clinical management after resection and improve decision-making prior to transplantation.

Utilizing a newly developed SK-N-AS xenograft model we show effective tumor targeting of the human aGD2-hSIRPα fusion mAbs with hSIRPα in a C-terminal configuration. These data provide the first proof of principal for NB tumor targeted blockade of CD47 by aGD2-hSIRPα fusion mAbs in-vivo and support the further development of aGD2-hSIRPα mAbs as attractive therapeutics to improve aGD2 based NB immunotherapy.

Importantly, we have uncovered that CD47 stabilizes ROBO2 by sequestering the E3 ubiquitin ligase ITCH, thereby blocking ubiquitination and proteasomal degradation of ROBO2. These findings establish CD47 as a key regulator of GBM cell plasticity and highlight the therapeutic potential of targeting CD47-ROBO2 signaling in GBM.

P1/2, N=80, Recruiting, ALX Oncology Inc. | Not yet recruiting --> Recruiting

Furthermore, various novel therapeutic strategies-including small-molecule inhibitors, bispecific antibodies, nanoparticle-based agents, and combination therapies-are advancing SIRPα-targeted treatment beyond traditional blockade. These advances move toward precise, synergistic immunotherapy with broad clinical potential.

Multiple CD47/SIRP⍺-targeting therapeutics and multiple clinical trials have demonstrated encouraging results in patients with non-Hodgkin lymphoma, where objective responses have been observed in combination with rituximab and other anti-cancer agents. Next-generation approaches, such as bispecific antibodies and engineering efforts to reduce blood cell binding, are now under clinical development and may be successful strategies to unlock the extraordinary potential of the CD47/SIRP⍺ immune checkpoint.

CD47 might be involved in the disease progression and prognosis of CHL, it had a closely positive correlation with PD-L1. Targeting of CD47 and PD1/PDL1 might provide a promising strategy in CHL.

MDA-MB-231 cells were treated with doxorubicin (DOX), polygodial (PG), or both, and CD47/CALR expression was analyzed at sublethal concentrations determined via MTT assay...Combination treatment of (DOX + PG), as well as co-loaded NPs, significantly decreased CD47 and CALR levels, reversing CD47 and CALR elevation that acts as a surrogate immunosurveillance marker and enhancing the CALR/CD47 surface expression ratio. These findings suggest a promising strategy for further examination and dose optimization in vivo studies for metastasis inhibition and as maintenance therapy.

While ELO alone has shown modest single agent activity, combination with immunomodulatory drugs (IMIDs), such as lenalidomide and pomalidomide (POM), has proven beneficial in treating MM. NK cells exposed to the TCSCTX or CTX+POM from MM cells potentiated NK cell cytotoxicity of MM cells and induced expression of PD-L1 and CD47 on MM cells. Dual targeting of PD-L1 and CD47 using anti-PD-1 and an anti-CD47 antibody significantly enhanced NK cytotoxicity and secretion of anti-tumour effector molecules, TNF-α and granzyme B. These findings support the addition of CTX to ELO-containing MM regimens and provide a rationale for combining POM with immune checkpoint blockade to maximise NK cytotoxicity against MM.