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Expandable Myeloid Progenitors Enable Engineered Immunotherapy

Expandable myeloid progenitors enable engineered immunotherapy by shifting cell therapy upstream from short-lived mature macrophages or neutrophils to renewable granulocyte-monocyte progenitors and other bioengineered myeloid precursors. This strategy addresses limits of mature myeloid cell therapy, including poor ex vivo expansion, genetic tractability, and biodistribution after transfer, while preserving myeloid differentiation potential for tumor-infiltrating macrophages and related effector cells[1][2][3].

Mechanistically, defined culture conditions can support long-term expansion of mouse and human granulocyte-monocyte progenitors while preserving progenitor identity and myeloid potential. Myeloperoxidase regulates GMP proliferation, and transferred expanded GMPs seed hematopoietic niches, generate donor-derived myelopoiesis, and produce abundant tumor-infiltrating macrophages. CAR-engineered GMPs suppress CD19-positive leukemia and HER2-positive solid tumors, while CAR-Fc designs recruit host Fc receptor-expressing phagocytes, enable T-cell priming across MHC mismatch, and enhance allogeneic antitumor activity[1].

Disease applications now center on scalable cancer immunotherapy, solid-tumor targeting, allogeneic "off-the-shelf" cell products, infectious-disease repair, and myeloid payload delivery. Human CAR macrophages showed antigen-specific phagocytosis and tumor clearance, reduced tumor burden, prolonged survival in solid-tumor xenograft models, and induced a pro-inflammatory tumor microenvironment. iPSC-derived CAR macrophages and hPSC-CAR macrophages extend the platform by enabling renewable manufacturing, stable CAR expression, innate immune activation, and improved antitumor activity. CAR-neutrophil systems further show how engineered myeloid lineages can cross barriers and deliver tumor-microenvironment-responsive nanodrugs in glioblastoma models[3][4][5][6][7].

Key gaps involve persistence, differentiation control, inflammatory toxicity, allogeneic compatibility, tumor education, manufacturing reproducibility, and proof of clinical benefit. Future work should define optimal progenitor stage, CAR signaling modules for myeloid biology, Fc receptor engagement, safety switches, lineage-restricted differentiation, and combinations with checkpoint blockade or cytokine engineering. The strongest prospect is a scalable engineered-myeloid platform that continuously supplies tumor-homing innate immune cells while coordinating adaptive immunity in tumors that resist conventional CAR-T therapy[1][2][3][5][6].

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Cat. No. Product Name Information Application Publication
HY-N0762 Isobavachin
Isobavachin is an orally active, blood-brain barrier-penetrating prenylated flavonoid present in Psoralea corylifolia. Isobavachin inhibits human CYP2B6, CYP2C9, CYP2C19, UGT1A1, UGT1A9, and UGT2B7. Isobavachin suppresses MAPK activation, NF-κB nuclear translocation, overexpression of iNOS/COX-2, FcεRI-mediated signaling pathways, and RANKL-induced osteoclastogenesis. Isobavachin induces autophagy, cytotoxicity, neuronal differentiation, and NRF2 activation; it alleviates oxidative damage, inflammatory responses, apoptosis, iron accumulation, mitochondrial biogenesis, and mast cell degranulation. Isobavachin is applicable to research related to liver injury, inflammatory diseases, osteoporosis, liver cancer, prostate cancer, glioma, periodontitis-induced bone loss, and Alzheimer's disease.
6
HY-P99979 Rat IgG1 kappa, Isotype Control
Rat IgG1 kappa, Isotype Control, a rat monoclonal antibody, is an isotype control for Rat IgG1κ antibody.
3
HY-P99037 Nipocalimab
Nipocalimab (M281) is a fully humanized, recombinant, and non-glycosylated IgG1 monoclonal antibody. Nipocalimab can bind to the IgG-binding site of FcRn with high affinity and inhibit the transplacental transfer of IgG. Nipocalimab can be used in the research of fetal and neonatal hemolytic disease, myasthenia gravis, and various IgG-mediated autoimmune diseases.

Species: Human

3
HY-P9963 Blinatumomab
Blinatumomab (Anatumomab) is a bispecific monoclonal antibody with two binding sites, one for CD3E on T cells and one for CD19 on B cells. Blinatumomab can be used in research for acute lymphoblastic leukemia.

Species: Human

CD19  
Cancer  
3
HY-P99711 Loncastuximab
Loncastuximab (RB4v1.2) is an anti-CD19 monoclonal antibody. Loncastuximab has antitumor activity and can be used in the research of Non-Hodgkin Lymphoma (NHL) and Diffuse Large B-cell Lymphoma (DLBCL). Loncastuximab is capable of synthesizing the ADC molecule Loncastuximab tesirine (HY-P99349).

Species: Human

Cancer  
2
HY-P99285 Denintuzumab
Denintuzumab (hBU 12) is a recombinant humanized anti-CD19 monoclonal antibody. Denintuzumab binds to CD19 on the surface of B cells. Denintuzumab can be used as the antibody moiety (ADC antibody) of antibody-drug conjugates to synthesize ADC, Denintuzumab Mafodotin (SGN-CD19A). Denintuzumab Mafodotin can be used in the research of acute lymphoblastic leukemia.

Species: Human

1
HY-153084A CD19 CAR mRNA (Human)
CD19 CAR mRNA (Human) expresses CAR protein that specifically targets human CD19. CD19 CAR mRNA can trigger transitory expression of CAR, allowing T cells to be targeted without permanent genetic modification. CD19 CAR mRNA targets CD19 which is a transmembrane glycoprotein primarily expressed on B lymphocytes and is important in B cell activation. CD19 CAR mRNA can be studied in cancer research such as lymphoma and leukemia.
mRNA   CD19  
Cancer  
1
HY-P99300 Ligelizumab
Ligelizumab (QGE 031) is a humanized high-affinity anti-immunoglobulin IgE monoclonal antibody. Ligelizumab selectively inhibits the binding of IgE to the high-affinity receptor FcεRI, while the inhibitory effect on the low-affinity receptor CD23 is weak. Ligelizumab can inhibit the activation of effector cells such as mast cells and Basophil, while reducing the production of IgE by B cells, and restoring the IFN-α production and regulatory T cell (Treg) induction function of plasmacytoid dendritic cells (pDC). Ligelizumab can be used in the study of allergic diseases (such as chronic spontaneous urticaria, allergic asthma).

Species: Human

1
HY-P99014 Cusatuzumab
Cusatuzumab (ARGX-110) is a selective competitive blocker targeting CD70 (with an equilibrium dissociation constant of 17 pM for binding to human CD70). Cusatuzumab also possesses enhanced antibody-dependent cell-mediated cytotoxicity (ADCC) activity. It is a humanized IgG1 monoclonal antibody, artificially synthesized through humanization and genetic engineering modifications (CH2 region mutation to enhance effector function). Cusatuzumab has a dual mechanism of action: firstly, it competitively blocks the interaction between CD70 and CD27, inhibiting the CD27-NF-κB signaling pathway, reducing regulatory T cell (Treg) activation and tumor cell proliferation; secondly, by enhancing binding to FcγRIIIa, it mediates ADCC and antibody-dependent cellular phagocytosis (ADCP), directly lysing CD70-positive tumor cells. Cusatuzumab can efficiently eliminate leukemia stem cells (LSCs), induce tumor cell differentiation and apoptosis, restore immune surveillance, and target CD70-positive tumors. Cusatuzumab is used in the study of acute myeloid leukemia (AML).

Species: Human

1
HY-P99113 Inebilizumab
Inebilizumab is an anti-CD19 monoclonal antibody (mAb) with enhanced antibody-dependent cell-mediated cytotoxicity against B cells. Inebilizumab can be used for multiple sclerosis and neuromyelitis optica research.

Species: Human

1
HY-P99976 Anti-Mouse CD19 Antibody (1D3)
Anti-Mouse CD19 Antibody (1D3) is an IgG2a antibody inhibitor targeting mouse CD19. Anti-Mouse CD19 Antibody (1D3) reduces CD19 expression levels on the surface of B cells. Anti-Mouse CD19 Antibody (1D3) inhibits the replication of peritoneal B-1a cells.

Species: Mouse

/
HY-P99313 Quilizumab
Quilizumab (Anti-Human IGHE Recombinant Antibody; 47H4; MEMP1972A) is a monoclonal antibody that targets FcγRIIIa and the M1 prime segment of human membrane-bound IgE. Quilizumab has enhanced FcγRIIIa binding affinity and activity against IgE class-switched B cells, and reduces serum IgE levels by inducing antibody-dependent cell-mediated cytotoxicity and apoptosis through cross-linking of membrane-bound IgE receptors. Quilizumab depletes IgE-producing cells; it also directly binds the membrane-bound M1 prime domain on IgE class-switched cells to inhibit IgE production. Quilizumab is used in research on allergic asthma and allergic diseases (asthma, allergic rhinitis).

Species: Human

/
HY-P99113A Inebilizumab (FUT8-KO)
Inebilizumab (FUT8-KO) is an anti-CD19 monoclonal antibody expressed by CHO cells with the fucosyltransferase 8 gene (FUT8) knocked out. Fucose deficiency enhances the antibody-dependent cellular cytotoxicity (ADCC) effect of the antibody.Inebilizumab (FUT8-KO) exhibits enhanced ADCC against B cells and can be used for research on multiple sclerosis and neuromyelitis optica.

Species: Human

/
HY-P99125 Anti-Mouse CD16/CD32 Antibody (2.4G2)
Anti-Mouse CD16/CD32 Antibody (2.4G2) is an anti-mouse CD16/CD32 IgG2b monoclonal antibody. Anti-Mouse CD16/CD32 Antibody (2.4G2) can block Fcγ receptor-mediated immune responses. Anti-Mouse CD16/CD32 Antibody (2.4G2) can block the combination of CD16 and FcγRs to reduce the production of foam cells. Anti-Mouse CD16/CD32 Antibody (2.4G2) can be used for researches on atherosclerosis and autoimmune hematological disorders.

Species: Mouse

/
HY-P990091 Riliprubart
Riliprubart (SAR 445088) is a selective anti-C1s humanized IgG4 monoclonal antibody with mutations that enhance its binding to the neonatal Fc receptor. Riliprubart blocks activation of the classical complement pathway, prevents the formation of the C3 convertase C4b2a, and inhibits complement-mediated hemolytic activity. Riliprubart can be used in research related to classical complement-mediated diseases, cold agglutinin disease, and chronic inflammatory demyelinating polyneuropathy. For the isotype control of Riliprubart, refer to Human IgG4 (S228P) kappa, Isotype Control (HY-P99003).

Species: Human

/
HY-P99868 Duvortuxizumab
Duvortuxizumab (MGD 011) is a chimeric humanized IG antibody targeting CD19 and CD3E.

Species: Human

CD19   CD3  
Cancer  
/
HY-P99761 Obexelimab
Obexelimab (XmAb5871) is a humanized anti-CD19 antibody. Obexelimab works by inhibiting B cell receptor (BCR) mediated calcium influx and promoting the phosphorylation of Fc γ receptor IIb (FcγRIIb), which reduces B cell activation and function, leading to B cell apoptosis. Obexelimab can be used in research for rheumatoid arthritis and systemic lupus erythematosus.

Species: Human

/
HY-P991028 Surovatamig
Surovatamig (AZD0486; TNB-486) is a fully human anti-CD19/CD3 IgG4 bispecific antibody. Surovatamig triggers T cell activation, releases cytotoxic granules, and induces T cell-dependent cellular cytotoxicity and tumor cell lysis. Surovatamig can reduces release of pro-inflammatory cytokines including IL-2, IFNγ, TNF. Surovatamig can be used for the research of cancer, such as B cell non-Hodgkin lymphoma.

Species: Human

/
HY-P99009 Batoclimab
Batoclimab (RVT-1401) is a fully humanized IgG1 monoclonal antibody targeting FcRn. Batoclimab has high affinity for the IgG-binding site on FcRn. By competitively binding to the IgG binding site on FcRn, Batoclimab blocks FcRn-mediated recycling of IgG, resulting in enhanced degradation and subsequent reductions in IgG levels. Batoclimab can be used in the research of autoimmune diseases such as myasthenia gravis and thyroid eye disease.

Species: Human

/
HY-147305 Efgartigimod alfa
Efgartigimod alfa (ARGX-113) is a reversibility, humanized Fc receptor antagonist . Efgartigimod alfa is a anti FcRn monoclonal immunoglobulin G (IgG1) Fc fragment. Efgartigimod reduces serum levels of total IgG, including pathogenic autoantibodies, by blocking FcRn function without permanent impairment. Efgartigimod alfa can be used for generalised myasthenia gravis (gMG) and primary immune thrombocytopenia research.

Species: Human

/

Keywords

expandable myeloid progenitors, granulocyte-monocyte progenitors, engineered immunotherapy, CAR macrophages, CAR-Fc, CAR neutrophils, allogeneic cell therapy, tumor microenvironment