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CD47 is the 'don't eat me' signal: it binds SIRP-alpha on macrophages to stop them engulfing the cell, and over 90% of AML blasts and large B-cell lymphoma cells display it. Blocking it should let macrophages eat tumour cells, but red cells carry CD47 too, so anaemia is built in, and the lead antibody magrolimab was dropped after failed trials. This dossier gathers the 4 products (0 approved), 11 trials, 4 pathways and 0 resistance routes in the corpus that involve it, with external identifiers so it can be joined to UniProt, ChEMBL, Open Targets and the rest of biology.
Binds SIRPα on macrophages to inhibit phagocytosis; ubiquitous on red cells, causing anaemia.
| Cancer | Prevalence | Measure | Note | Source |
|---|---|---|---|---|
| Acute myeloid leukaemia | >90% | Surface expression on blasts | Magrolimab discontinued | Wikipedia |
| Diffuse large B-cell lymphoma | >90% | Surface expression | Wikipedia |
Approximate, population-level figures; the measure column says what was counted. Ranges show the midpoint as a bar.
| Modality | Phase 3 | Phase 2 | Withdrawn or failed |
|---|---|---|---|
| Antibody 2 | - | ||
| Bispecific antibody 2 | - | - |
| Trial | Setting | Result | Products | ||
|---|---|---|---|---|---|
| 3 | - | A Phase 3, Randomized, Open-Label Study Evaluating the Safety and Efficacy of Magrolimab in Combination With Azacitidine Versus Physician's Choice of Venetoclax in Combination With Azacitidine or Intensive Chemotherapy in Previously Untreated Patients With TP53 Mutant Acute Myeloid Leukemia | - | ||
| 3 | - | A Phase 3, Randomized, Double-Blind, Placebo-Controlled Study Evaluating the Safety and Efficacy of Magrolimab Versus Placebo in Combination With Venetoclax and Azacitidine in Newly Diagnosed, Previously Untreated Patients With Acute Myeloid Leukemia Who Are Ineligible for Intensive Chemotherapy | - | ||
| 3 | - | ENHANCE: A Randomized, Double-blind, Multicenter Study Comparing Magrolimab in Combination With Azacitidine Versus Azacitidine Plus Placebo in Treatment-naïve Patients With Higher Risk Myelodysplastic Syndrome | - | ||
| 3 | Recruiting | A Randomized, Controlled, Multicenter Phase 3 Study of AK112 in Combination With AK117 Versus Pembrolizumab as First Line Treatment for a Programmed Cell Death-ligand 1 (PD-L1) Positive Population With Recurrent or Metastatic Head and Neck Squamous Cell Carcinoma (R/M HNSCC) | - | ||
| 2 | Active | A Phase II Study of AK112 With or Without AK117 for Patients With Metastatic Colorectal Cancer | - | ||
| 2 | Active | A Phase II Study of AK117/AK112 in Combination With Chemotherapy for Patients With Previously Untreated Metastatic Triple-Negative Breast Cancer | - | ||
A Study of Ivonescimab in First-Line ES-SCLC NCT07245446 | 2 | Recruiting | A Phase II Clinical Study of Ivonescimab Combination Therapy as First-Line Treatment for Extensive-Stage Small Cell Lung Cancer (ES-SCLC) | - | |
| 1/2 | Active | A Phase Ib/II Study of AK112#PD-1/VEGF Bispecific Antibody# in Combination With AK117#Anti-CD47 Antibody# in Advanced Malignant Tumors | - | ||
| 1/2 | Recruiting | An Open-label, Multicenter, Dose Escalation, and Dose Expansion Phase 1/2 Study With Peluntamig (PT217) Followed by a Key ChemotherapY and/or Checkpoint Inhibitor ComBination in Patients With NeuRoendocrIne Carcinomas That Are Known to be DLL3 expressinG CancErs (SKYBRIDGE) | - | ||
| 1/2 | Active | A Phase Ib/II Trial of AK117 (Anti-CD47 Antibody) in Patients With Acute Myeloid Leukemia | - | ||
| 1/2 | Recruiting | A Phase 1/2, Open-Label, Dose Escalation and Expansion Study With PT886 (Spevatamig) Followed by a Multi-cohorT Study in Patients With Advanced GastrIc, Gastroesophageal JuNction, Pancreatic Ductal or Biliary Tract AdEnocarcinomas of PT886, in Combination With ChemotherApy, and/or an Immune ChecKpoint Inhibitor. The TWINPEAK Study | - |
No recorded escape route names this target.
Macrophages eat cells that look wrong unless the cell shows CD47, a 'don't eat me' badge that binds SIRP-alpha. Leukaemias, myelodysplastic syndromes, lymphomas and carcinomas overproduce CD47 to escape being eaten; antibodies that cover the badge work in the lab, but the leading drug, magrolimab, failed in blood cancers because red cells wear the same badge and lose it too.
Which nodes have drugs →MYC is the most commonly amplified cancer gene, a master switch that turns on thousands of growth genes. It has no pocket for a conventional drug, so it remained 'undruggable' for 40 years; the first direct MYC drugs finally entered trials in the 2020s.
Which nodes have drugs →Tumours recruit the body's clean-up cells (macrophages and immature myeloid cells) and re-train them as bodyguards. They switch off T cells, build vessels, and, when a therapeutic antibody flags a cancer cell for eating, are told 'don't eat me' by CD47 on its surface.
Which nodes have drugs →A tumour is not just cancer cells. It is a neighbourhood of fibroblasts, immune cells, blood vessels, nerves, and scaffolding that the cancer recruits and corrupts, and that decides whether drugs and immune cells can get in.
Which nodes have drugs →No companion diagnostic in the registry measures this target.
No model entry for this target yet; check the cancer entries on the models page.
No open questions recorded for this target yet. Suggest one.
Query for this target: (TITLE:"CD47" OR ABSTRACT:"CD47") AND (cancer OR tumor OR tumour OR oncology OR carcinoma OR lymphoma OR leukemia OR leukaemia OR myeloma OR sarcoma OR melanoma OR glioma). Results are unfiltered search hits about CD47, not a curated reading list.
The dossier as machine-readable JSON, at /api/v1/dossiers/cd47.json: identifiers from HGNC, Ensembl, UniProt and ChEMBL, products with status, trials, pathways, hotspots, open questions and assays. The full entity record is in the open API at /api/v1/entities/cd47.json. Licence CC BY-NC 4.0.