Substances tested

What has been given to the plasmocyte, and what the plasmocyte did. Research reference, not medical advice.

All substances 16

Bortezomib proteasome inhibitor, reversible boronic acid

acts on 20S proteasome, beta-5 subunit

Blocks proteasomal degradation of misfolded immunoglobulin chains. The plasmocyte already runs its endoplasmic reticulum near capacity, so the undegraded load tips it into terminal ER stress and apoptosis. This is why the cell that secretes the most protein is the cell most sensitive to proteasome inhibition. First proteasome inhibitor approved, 2003.

dose: not stated in the abstract · human, multiple myeloma · review of mechanism, resistance patterns and combination regimens · Ito S 2020, Cancers: Proteasome Inhibitors for the Treatment of Multiple Myeloma · source

Carfilzomib proteasome inhibitor, irreversible epoxyketone

acts on 20S proteasome, beta-5 subunit, selective

Binds the beta-5 subunit irreversibly rather than reversibly, giving more sustained proteasome blockade than bortezomib and activity in bortezomib-refractory disease.

dose: not stated in the abstract · human, relapsed and refractory multiple myeloma · review · Ito S 2020, Cancers: Proteasome Inhibitors for the Treatment of Multiple Myeloma · source

Ixazomib proteasome inhibitor, oral boronic acid

acts on 20S proteasome, beta-5 subunit

The first orally available proteasome inhibitor, same mechanistic class as bortezomib.

dose: not stated in the abstract · human, multiple myeloma · review · Ito S 2020, Cancers: Proteasome Inhibitors for the Treatment of Multiple Myeloma · source

Lenalidomide immunomodulatory drug (IMiD)

acts on cereblon, substrate receptor of the CRL4-CRBN ubiquitin ligase

Binds cereblon and redirects the CRL4-CRBN ubiquitin ligase onto IKZF1 (Ikaros) and IKZF3 (Aiolos), transcription factors the myeloma plasmocyte needs to survive. Degrading them kills the cell. Intrinsic and acquired loss of cereblon is the main route to resistance.

dose: not stated in the abstract · human, multiple myeloma · review of mechanism and clinical experience · Holstein SA, McCarthy PL 2017, Drugs: Immunomodulatory Drugs in Multiple Myeloma · source

Thalidomide immunomodulatory drug (IMiD)

acts on cereblon, CRL4-CRBN ubiquitin ligase

Same cereblon-directed mechanism as lenalidomide and pomalidomide: degradation of IKZF1 and IKZF3.

dose: not stated in the abstract · human, multiple myeloma · review · Holstein SA, McCarthy PL 2017, Drugs: Immunomodulatory Drugs in Multiple Myeloma · source

Pomalidomide immunomodulatory drug (IMiD)

acts on cereblon, CRL4-CRBN ubiquitin ligase

Same cereblon-directed degradation of IKZF1 and IKZF3; used in later lines, including after lenalidomide.

dose: not stated in the abstract · human, multiple myeloma · review · Kulig P et al. 2023, Cancers: Lenalidomide in Multiple Myeloma, Review of Resistance Mechanisms, Current Treatment Strategies and Future Perspectives · source

Daratumumab anti-CD38 monoclonal antibody, humanised IgG1 kappa

acts on CD38, constitutively high on the plasmocyte from the plasmablast stage onward

Kills the plasmocyte by complement-dependent cytotoxicity and antibody-dependent cell-mediated cytotoxicity; bone marrow stromal cells do not block either. Separately, it depletes CD38-positive regulatory T cells, regulatory B cells and myeloid-derived suppressor cells, relieving immunosuppression and expanding T cell numbers in treated patients.

dose: 16 mg/kg monotherapy in the phase II trial cited at first approval, giving about 30 percent overall response · human, multiple myeloma; in vitro and patient samples · CDC and ADCC assays; flow cytometry and T cell repertoire sequencing in treated patients · de Weers M et al. 2011, J Immunol; mechanism. Immunosuppressive cell depletion: Krejcik J et al. 2016, Blood, https://pubmed.ncbi.nlm.nih.gov/27222480/ . First approval and dose: McKeage K 2016, Drugs, https://pubmed.ncbi.nlm.nih.gov/26729183/ · source

Isatuximab anti-CD38 monoclonal antibody

acts on CD38, at an epitope distinct from the daratumumab epitope

Binds CD38 non-competitively with respect to daratumumab: epitope mapping places the two on distinct, non-overlapping epitopes, which raises the possibility of sequential use.

dose: not stated in the abstract · human, multiple myeloma · epitope mapping · Non-Competitive Binding of Isatuximab and Daratumumab to CD38, PMC12566780 · source

Teclistamab bispecific antibody, BCMA x CD3

acts on BCMA (TNFRSF17) on the plasmocyte, CD3 on T cells

Bridges a T cell to the plasmocyte through BCMA, which is expressed almost exclusively on plasmocytes and plasmablasts. MajesTEC-1 reported 63 percent overall response with 39 percent at or above complete response. Loss of BCMA and T cell exhaustion are the principal resistance routes.

dose: not stated in the abstract · human, relapsed or refractory multiple myeloma · clinical trial review; longitudinal resistance analysis · Piron B 2026, Biologics Targets and Therapy: Teclistamab for Relapsed or Refractory Multiple Myeloma. Resistance: Vishwamitra D 2026, Haematologica, https://pubmed.ncbi.nlm.nih.gov/42273947/ · source

Elranatamab bispecific antibody, BCMA x CD3

acts on BCMA on the plasmocyte, CD3 on T cells

Same BCMA-directed T cell engagement as teclistamab. The MagnetisMM-1 phase 1 dose-escalation reported 64 percent overall response in triple-class-refractory patients; extended MagnetisMM-3 follow-up confirms durable responses.

dose: recommended dose established in the phase 1 dose escalation; the value is not stated in the abstract · human, relapsed or refractory multiple myeloma · phase 1 dose-escalation trial; extended follow-up · Bahlis NJ 2023, Nat Med: Elranatamab in relapsed or refractory multiple myeloma, the MagnetisMM-1 phase 1 trial. Follow-up: Tomasson MH 2024, HemaSphere, https://pubmed.ncbi.nlm.nih.gov/39055646/ · source

Ciltacabtagene autoleucel BCMA-directed autologous CAR T cell therapy

acts on BCMA, engaged by two distinct BCMA-binding single-chain variable domains with 4-1BB co-stimulation

A single infusion produced 97.9 percent overall response and 82.5 percent stringent complete response at two-year follow-up in heavily pretreated patients (CARTITUDE-1), and 84.6 percent overall response in CARTITUDE-4. FDA approved 2022, extended to 1 to 2 prior lines in 2024.

dose: single infusion; cell dose not stated in the abstract · human, relapsed or refractory multiple myeloma · phase 1b/2 trial with two-year follow-up · Martin T 2023, J Clin Oncol: Ciltacabtagene Autoleucel for Relapsed/Refractory Multiple Myeloma, CARTITUDE-1. Discovery and development: Strassl I 2024, Expert Opin Drug Discov, https://pubmed.ncbi.nlm.nih.gov/38369760/ · source

Idecabtagene vicleucel BCMA-directed autologous CAR T cell therapy

acts on BCMA

The pivotal KarMMa phase 2 trial reported 73 percent overall response and 33 percent complete response, leading to the first CAR T approval in myeloma.

dose: single infusion; cell dose not stated in the abstract · human, relapsed and refractory multiple myeloma · phase 2 trial · Munshi NC et al. 2021, N Engl J Med: Idecabtagene Vicleucel in Relapsed and Refractory Multiple Myeloma · source

Interleukin-6 cytokine, physiological

acts on IL-6 receptor alpha (CD126) paired with gp130

Marrow stromal IL-6 drives STAT3 activation in the plasmocyte, promoting survival, proliferation and protection from apoptosis. In myeloma an autocrine IL-6 loop makes this a therapeutic target. IL-6 is required for normal induction of a plasma cell response but not for its maintenance, so its effect is redundant with other niche signals.

dose: not stated in the abstract · human myeloma cells; mouse for the induction and maintenance distinction · receptor complex and signalling studies; IL-6-deficient mice · Barillé S et al. 2000, Eur Cytokine Netw. Induction versus maintenance: Cassese G et al. 2003, J Immunol, https://pubmed.ncbi.nlm.nih.gov/12902466/ · source

APRIL and BAFF TNF-family ligands, physiological

acts on BCMA (TNFRSF17)

Bind BCMA on plasmocytes and plasmablasts and trigger NF-kB and PI3K survival signalling. BCMA expression is near-exclusive to this lineage, which is what makes it a clean therapeutic target.

dose: not stated in the abstract · human, multiple myeloma · expression and signalling analysis · Novak AJ et al. 2004, Blood: Expression of BCMA, TACI, and BAFF-R in multiple myeloma · source

Oligomeric APRIL and BAFF TNF-family ligands, physiological

acts on TACI (TNFRSF13B)

TACI is activated solely by the oligomeric forms of BAFF and APRIL, unlike BAFF-R which responds to the monomer. This supports survival of activated B cells and plasmablasts at germinal centre exit. Loss-of-function TACI mutations cause common variable immunodeficiency.

dose: not stated in the abstract · human and mouse · receptor activation assays with defined ligand oligomeric states · Bossen C et al. 2008, Blood: TACI, unlike BAFF-R, is solely activated by oligomeric BAFF and APRIL · source

CXCL12 (SDF-1 alpha) chemokine, physiological

acts on CXCR4

Stromal CXCL12 holds the plasmocyte in its marrow survival niche through CXCR4. Disrupting the axis mobilises plasmocytes out of the marrow into circulation, which is how plerixafor is used to mobilise myeloma cells. CXCL12 also acts as one of the synergistic survival signals of the niche.

dose: not stated in the abstract · mouse, NZB/W · homing and survival studies · Cheng Q et al. 2018, Eur J Immunol: CXCR4-CXCL12 interaction is important for plasma cell homing and survival · source

Substances that act on the plasmocyte, whether normal or malignant. Every row rests on a PubMed abstract. A dose the abstract does not state is written as such, never guessed. Where a number comes from malignant plasmocytes the species and method columns say so, and it is not mixed with normal-plasmocyte values. Most of the pharmacology of this cell is written in the myeloma literature, which is why so many rows are drawn from it. Research reference, not medical advice. Verification: all 18 PubMed ids in this file were run through check-pubmed.py on 2026-09-12 and every title matched the claim hung on it. That run caught two author attributions written from memory rather than read from the record, Gandolfi for what is Ito S 2020 and Costa for what is Kulig P 2023; both are corrected here and every other cite line was rewritten to the author, year and journal NCBI returns. This file is seeded from audited sources and will be extended from the sweep corpus.