Antibody-drug conjugates
A carrier that finds the cell, a linker that lets go at the right moment, and a payload that does the killing; the drug-to-antibody ratio says how many payloads ride along. Peptide and bicyclic conjugates and protein-toxin fusions are here too, since they swap the carrier and keep the idea. The grid below is target against payload class: 31 by 6 from 78 medicines, 15 combinations approved, 29 in development, 6 tried and stopped, 149 untried in this corpus.
Antibody-drug conjugatesRadioligandsCAR cell therapiesTCR-T cell therapiesBispecific antibodiesDegraders and molecular gluesSmall-molecule inhibitorsNaked antibodiesCytokinesCancer vaccinesOncolytic virusesOther cell therapies
Approved 15In development 29Tried and stopped 6Recorded, state unclear 0Untried here 14931 target rows x 6 payload class columns. Click a cell to filter the table.
Every tried combination
50 combinations
(showing the first 30)
Stopped, and why
6 medicines recorded as stopped; 22 recorded reasons, including stopped studies of medicines still in development- Anetumab ravtansineTried and stopped
Anetumab ravtansine was the first antibody-drug conjugate tested in a randomised trial in mesothelioma, aimed at the mesothelin protein that nearly all mesotheliomas carry; it was no better than vinorelbine chemotherapy as second-line treatment, and is now being tried with pembrolizumab.
- Anetumab ravtansineTried and stopped
PFS 4.3 vs 4.5 months, HR 1.22; primary endpoint not met.
Anetumab ravtansine versus vinorelbine in relapsed mesothelin-positive pleural mesothelioma: phase 2, negative · trial record
- Depatuxizumab mafodotinTried and stopped
Depatuxizumab mafodotin carried a cell-killing payload to glioblastomas with extra copies of the EGFR gene. It caused serious eye problems and, in the phase 3 INTELLANCE-1 trial, did not help patients live longer, so development stopped in 2019.
- Depatuxizumab mafodotinTried and stopped
Depatuxizumab mafodotin added to radiotherapy and temozolomide did not improve overall survival in EGFR-amplified glioblastoma; stopped for futility.
INTELLANCE-1: phase 3, negative · trial record
- Moxetumomab pasudotoxTried and stopped
An immunotoxin for hairy cell leukaemia that produced lasting remissions in relapsed patients but was withdrawn from sale in 2023 for commercial reasons.
- Moxetumomab pasudotoxTried and stopped
Lumoxiti accelerated approval Sep 2018; discontinued by AstraZeneca and withdrawn 2023
FDA (US): withdrawn 2023 · regulator row
- Moxetumomab pasudotoxTried and stopped
Authorised 8 Feb 2021; marketing authorisation withdrawn at the holder's request 23 Jul 2021
EMA / European Commission (EU): withdrawn 2021 · regulator row
- Rovalpituzumab tesirineTried and stopped
Rovalpituzumab tesirine (Rova-T) was the first drug against DLL3 in small-cell lung cancer. AbbVie bought it for $5.8B and abandoned it after two failed phase 3 trials. The target later worked with a different weapon.
- Trastuzumab duocarmazineTried and stopped
A HER2 ADC with a DNA-alkylating payload that beat chemotherapy in a phase 3 trial yet never reached the market, because eye and lung toxicity and a stronger rival arrived first.
- Trastuzumab duocarmazineTried and stopped
Complete response letter May 2023 (Byondis)
FDA (US): rejected 2023 · regulator row
- Trastuzumab duocarmazineTried and stopped
Marketing authorisation application withdrawn before a CHMP opinion
EMA / European Commission (EU): withdrawn · regulator row
- Tusamitamab ravtansineTried and stopped
Tusamitamab ravtansine was Sanofi's ADC against the classic CEA tumour marker, stopped for futility in lung cancer in 2023.
- Patritumab deruxtecanIn development
BLA withdrawn May 2025 after CRL (manufacturing) and HERTHENA-Lung02 OS miss
FDA (US): withdrawn 2025 · regulator row
- Patritumab deruxtecanIn development
Complete response letter citing third-party manufacturing inspection
- Patritumab deruxtecanIn development
BLA withdrawn after HERTHENA-Lung02 met PFS but not OS
- Zelenectide pevedotinIn development
Programme deprioritised after regulatory feedback on Duravelo-2 design
- Belantamab mafodotinApproved
Withdrawn after DREAMM-3 failed to confirm benefit
- Belantamab mafodotinApproved
Complete response letter on combination filing; resubmitted
- Gemtuzumab ozogamicinApproved
Voluntary withdrawal after confirmatory trial showed no benefit and excess deaths
- Sacituzumab govitecanApproved
Urothelial cancer indication voluntarily withdrawn after TROPiCS-04
- Trastuzumab emtansineApproved
Trastuzumab emtansine did not improve overall survival over taxane chemotherapy in previously treated HER2-positive gastric cancer.
GATSBY: phase 2/3, negative · trial record
- Trastuzumab emtansineApproved
Pathological complete response 44.4% (T-DM1 + pertuzumab) vs 55.7% (TCHP); more locoregional progression before surgery with T-DM1.
KRISTINE: phase 3, negative · trial record
Proposed, not yet tried
20 proposals from the open pipeline, scored and searched (docs/OPEN-PIPELINE.md); hypotheses, not records of a medicineClinical evidence 6Preclinical 2No public evidence 8Already in development 4
| Score | Target | Payload class | Status | Rationale | Evidence | Now in the corpus |
|---|---|---|---|---|---|---|
| 84 | Nectin-4 | Topoisomerase I inhibitor | Already in development | Nectin-4 ADC with a topoisomerase-I payload. Nectin-4 is validated with a tubulin payload (enfortumab-vedotin) and the topoisomerase-I class is the best-validated ADC payload in the corpus (trastuzumab-deruxtecan, sacituzumab-govitecan, datopotamab-deruxtecan). The corpus holds a Nectin-4 x TROP2 bispecific ADC with a topoisomerase payload (ak146d1) and a Nectin-4 ADC in phase 3 whose payload the record does not state (shr-a2102), so the mono-specific Nectin-4 x topoisomerase-I cell reads as untried when the search shows it is occupied. Nectin-4 internalises (enfortumab-vedotin relies on it) and is expressed in breast, lung and pancreatic cancers beyond bladder; a topoisomerase-I payload would swap the neuropathy and skin toxicity of MMAE for the neutropenia and ILD class effects of camptothecins.Caveat: The corpus record for SHR-A2102 needs its payload class filled in; the open question is no longer whether the cell is tried but whether a topoisomerase-I Nectin-4 ADC works after enfortumab vedotin progression.Proposed by OnCo open pipeline, searched 2026-09-23. | Untried | |
| 83 | MET | Topoisomerase I inhibitor | Already in development | MET ADC with a topoisomerase-I payload. MET is validated by an approved tubulin ADC (telisotuzumab-vedotin) and kinase inhibitors (capmatinib, tepotinib), and topoisomerase-I payloads are approved on five antigens (trastuzumab-deruxtecan). The corpus holds a MET ADC in phase 3 whose payload the record does not state (telisotuzumab-adizutecan), so the MET x topoisomerase-I cell reads as untried when it is probably not. MET internalises and is over-expressed across lung, colorectal and gastric cancers beyond the amplified subset; a bystander-capable topoisomerase-I payload could reach MET-intermediate tumours that telisotuzumab-vedotin does not.Caveat: The corpus record for the phase-3 MET ADC needs its payload class filled in; if it is a topoisomerase-I inhibitor this cell is already occupied and the open question is how it sequences with the tubulin ADC.Proposed by OnCo open pipeline, searched 2026-09-23. | Now tried: see the cell | |
| 82 | Claudin 18.2 | Topoisomerase I inhibitor | Already in development | Claudin 18.2 ADC with a topoisomerase-I payload. Claudin 18.2 is validated by an approved antibody (zolbetuximab) and an approved CAR-T (satricabtagene-autoleucel), and the corpus holds a Claudin 18.2 ADC with a tubulin payload in phase 3 (cmg901). Several corpus Claudin 18.2 ADCs in phase 2 and 3 do not state their payload (ibi343, azd4360, xnw27011), so the Claudin 18.2 x topoisomerase-I cell reads as untried when it is almost certainly occupied. Claudin 18.2 is buried in tight junctions of normal stomach but exposed on cancer cells, giving a tumour-selective epitope; expression is heterogeneous, so a bystander-capable topoisomerase-I payload is the natural class.Caveat: This row is a data-quality flag as much as a proposal: the payload fields on the corpus Claudin 18.2 ADC records need filling before the engine can count this cell as in development.Proposed by OnCo open pipeline, searched 2026-09-23. | Now tried: see the cell | |
| 82 | EGFR | Topoisomerase I inhibitor | No public evidence | EGFR ADC with a topoisomerase-I payload. EGFR is validated by antibodies (cetuximab, amivantamab) and kinase inhibitors (osimertinib), and the corpus holds an EGFR ADC with a tubulin payload in phase 3 (mrg003) plus two bispecific EGFR ADCs with topoisomerase-I payloads (izalontamab-brengitecan, tilatamig-samrotecan). There is no mono-specific EGFR topoisomerase-I ADC in the corpus, the simplest construct in the family. EGFR internalises on antibody binding and is over-expressed in squamous cancers, but its expression on skin and gut means an EGFR ADC inherits cetuximab's rash plus payload toxicity; the corpus bispecific EGFR ADCs (izalontamab-brengitecan) use a second arm partly to bias delivery towards tumour.Caveat: The bispecific EGFR ADCs exist partly because a mono-specific EGFR ADC risks skin and gut toxicity at active doses; this proposal asks whether the simpler molecule can find a window, and depatuxizumab-mafodotin's failure in glioblastoma is a warning.Proposed by OnCo open pipeline, searched 2026-09-23. | Untried | |
| 81 | DLL3 | Topoisomerase I inhibitor | Already in development | DLL3 ADC with a topoisomerase-I payload. DLL3 is validated by an approved T-cell engager (tarlatamab) and a PBD ADC that reached phase 3 and was withdrawn for toxicity (rovalpituzumab-tesirine), while topoisomerase-I payloads are approved on five antigens (trastuzumab-deruxtecan, sacituzumab-govitecan). The corpus has a DLL3 ADC in phase 3 whose payload the record does not state (zl-1310), so the decomposer classes the DLL3 x topoisomerase-I cell as untried. DLL3 is tumour-restricted (no normal-tissue surface expression) and internalises, but at low density; a bystander-capable topoisomerase-I payload at DAR 8 fits low-density antigens far better than the DAR-2 PBD that failed with rovalpituzumab-tesirine.Caveat: The corpus DLL3 ADC record needs its payload filled in before this cell can be marked as in development; if the payload is a camptothecin, this proposal is already being tested rather than open.Proposed by OnCo open pipeline, searched 2026-09-23. | Untried | |
| 80 | TROP2 | Tubulin inhibitor | Clinical evidence | TROP2 ADC with a tubulin-inhibitor payload. TROP2 carries three approved topoisomerase-I ADCs (sacituzumab-govitecan, datopotamab-deruxtecan, sacituzumab-tirumotecan) and no tubulin-payload ADC in the corpus, while tubulin payloads are approved on Nectin-4 (enfortumab-vedotin) and HER2 (trastuzumab-emtansine). A tubulin-payload TROP2 ADC would give a second mechanism for the same antigen after topoisomerase-I failure, the sequencing already used across HER2 ADCs. TROP2 internalises and recycles quickly, which suits a permeable auristatin with bystander killing (bystander-effect); TROP2 on skin and mucosa predicts the rash and stomatitis already seen with the topoisomerase ADCs.Caveat: Earlier TROP2 auristatin conjugates were stopped in phase 1; the class may need a lower DAR or site-specific conjugation to be tolerable, and that history is the first thing to read.Proposed by OnCo open pipeline, searched 2026-09-23. | Untried | |
| 77 | Somatostatin receptor 2 | Topoisomerase I inhibitor | Clinical evidence | Somatostatin receptor 2 ADC with a topoisomerase-I payload. SSTR2 is validated by an approved radioligand (lutathera) and a phase-3 alpha emitter (ryz101), and topoisomerase-I payloads are the best-validated ADC class (trastuzumab-deruxtecan). No corpus product pairs SSTR2 with a cytotoxic payload, although the corpus already carries a bystander-capable topoisomerase payload family (topoisomerase-i-payloads) suited to heterogeneous receptor expression. SSTR2 is a G-protein-coupled receptor that internalises on agonist binding (the basis of lutathera); antibody-format ADCs against GPCRs are hard, so a peptide-drug conjugate with a camptothecin is the more plausible construct, and neuroendocrine tumours divide slowly.Caveat: Well-differentiated neuroendocrine tumours have low proliferation and replication-dependent poisons may add little to radioligand therapy; the better fit may be SSTR2-positive small-cell lung cancer, where cells divide fast.Proposed by OnCo open pipeline, searched 2026-09-23. | Untried | |
| 75 | HER2 | DNA crosslinker (PBD dimer) | Clinical evidence | HER2 ADC with a PBD dimer payload. HER2 is the most validated ADC target in the corpus, carrying a tubulin payload (trastuzumab-emtansine) and two topoisomerase-I payloads (trastuzumab-deruxtecan, trastuzumab-rezetecan), while the PBD dimer class is validated on CD19 (zynlonta). No corpus ADC combines HER2 with a DNA crosslinker, which would offer a mechanism unaffected by the topoisomerase-I resistance now emerging after deruxtecan exposure. HER2 internalises well (trastuzumab-emtansine, trastuzumab-deruxtecan), and a DAR-2 PBD dimer would not depend on high antigen density; but HER2 is expressed on cardiomyocytes and the gut, and PBD dimers carry fluid-retention and liver toxicity (pbd-dimer-payloads), so the therapeutic window is the open question.Caveat: A HER2 PBD ADC would need a therapeutic window that HER2 expression on normal heart and gut tissue may not allow; the tried-and-stopped history of HER2 PBD conjugates must be read before any new attempt.Proposed by OnCo open pipeline, searched 2026-09-23. | Untried | |
| 74 | PSMA | Topoisomerase I inhibitor | Preclinical | PSMA ADC with a topoisomerase-I payload. PSMA is validated by an approved radioligand (pluvicto) and three phase-3 alpha emitters (aaa817, ac225-psma), and topoisomerase-I is the dominant approved ADC payload class (trastuzumab-deruxtecan, sacituzumab-govitecan, datopotamab-deruxtecan). No corpus drug conjugates a PSMA antibody to a topoisomerase-I payload. Topoisomerase-I payloads kill more slowly dividing cells than auristatins and have bystander effect for heterogeneous PSMA expression; prostate cancer has had no camptothecin exposure, so no pre-existing resistance.Caveat: It would need to hold its own against a radioligand that already delivers a DNA-damaging dose to the same antigen; the likely place is after radioligand progression or in patients whose marrow reserve excludes further radiation.Proposed by OnCo open pipeline, searched 2026-09-23. | Untried | |
| 73 | CD19 | Topoisomerase I inhibitor | No public evidence | CD19 ADC with a topoisomerase-I payload. CD19 is validated as an ADC target with a PBD dimer (zynlonta), as a T-cell engager target (blinatumomab) and as a CAR-T target (tisagenlecleucel), while topoisomerase-I payloads dominate solid-tumour ADCs (trastuzumab-deruxtecan, sacituzumab-govitecan). No corpus ADC pairs CD19 with a topoisomerase-I payload; lymphoma cells proliferate fast enough for replication-dependent poisons to act. CD19 internalises (zynlonta depends on it) and is B-lineage restricted; a topoisomerase-I payload would give a lower-potency, higher-DAR alternative to the PBD dimer whose skin and fluid toxicities limit zynlonta.Caveat: A CD19 topoisomerase-I ADC would enter a field where CAR-T and CD20 x CD3 bispecifics already work; its niche would be outpatient, off-the-shelf therapy for patients unfit for those.Proposed by OnCo open pipeline, searched 2026-09-23. | Untried | |
| 72 | PSMA | Tubulin inhibitor | Clinical evidence | PSMA ADC with a tubulin-inhibitor payload. PSMA is validated by an approved radioligand (pluvicto) and tubulin payloads are approved on Nectin-4 (enfortumab-vedotin) and HER2 (trastuzumab-emtansine). No corpus ADC targets PSMA at all, although PSMA internalises and is the best-characterised antigen in prostate cancer. PSMA internalises through its cytoplasmic tail and is tumour-restricted apart from salivary glands, kidney and small bowel; an ADC would avoid the marrow and salivary dose of the radioligand, though prostate cancer grows slowly and tubulin agents need dividing cells.Caveat: Two earlier PSMA tubulin ADCs were stopped for neuropathy and neutropenia; a new attempt would need site-specific conjugation or a non-permeable payload to change the window.Proposed by OnCo open pipeline, searched 2026-09-23. | Untried | |
| 70 | CD79b | Topoisomerase I inhibitor | No public evidence | CD79b ADC with a topoisomerase-I payload. CD79b is validated by an approved tubulin ADC used in first-line lymphoma (polatuzumab-vedotin) and the topoisomerase-I class is the most validated payload family (trastuzumab-deruxtecan, sacituzumab-govitecan). No corpus ADC pairs CD79b with a topoisomerase-I payload. CD79b internalises via the B-cell receptor complex (polatuzumab-vedotin) and is B-lineage restricted; a topoisomerase-I payload would avoid the neuropathy of MMAE and could be combined with R-CHP where vincristine was dropped.Caveat: Polatuzumab already occupies first-line DLBCL; a second CD79b ADC would need a clean advantage, most plausibly activity after polatuzumab failure or a better neuropathy profile in older patients.Proposed by OnCo open pipeline, searched 2026-09-23. | Untried | |
| 69 | CD22 | DNA crosslinker (PBD dimer) | Clinical evidence | CD22 ADC with a PBD dimer payload. CD22 is validated with a DNA-cleaving calicheamicin payload (inotuzumab-ozogamicin) and the PBD dimer class is validated on the neighbouring B-cell antigen CD19 (zynlonta). No corpus ADC pairs CD22 with a PBD dimer, even though the two DNA-damaging classes have different resistance mechanisms. CD22 internalises rapidly (inotuzumab-ozogamicin) and both calicheamicin and PBD are DNA-damaging payloads that kill non-dividing blasts; the liver toxicity of both classes (veno-occlusive disease with inotuzumab) is the shared risk.Caveat: Both payload classes damage liver sinusoids; a CD22 PBD ADC would need to show it does not reproduce the veno-occlusive disease seen with inotuzumab before transplant.Proposed by OnCo open pipeline, searched 2026-09-23. | Untried | |
| 67 | BCMA | Topoisomerase I inhibitor | No public evidence | BCMA ADC with a topoisomerase-I payload. BCMA is validated across four formats in the corpus, including an ADC with a tubulin payload (belantamab-mafodotin), and the topoisomerase-I class is validated on solid-tumour antigens (trastuzumab-deruxtecan, sacituzumab-govitecan). No corpus ADC pairs BCMA with a topoisomerase-I payload, which would replace the ocular toxicity of MMAF with a different, better-understood profile. BCMA is plasma-cell restricted and internalises (belantamab-mafodotin); a permeable topoisomerase-I payload could avoid the corneal toxicity of MMAF, which is the dose-limiting problem of the approved BCMA ADC, but myeloma cells divide slowly, which blunts replication-dependent poisons.Caveat: Topoisomerase-I poisons need replicating cells; the low proliferative index of myeloma may make this class less active than in solid tumours, so a preclinical comparison against belantamab is the first step.Proposed by OnCo open pipeline, searched 2026-09-23. | Untried | |
| 67 | CD123 | Topoisomerase I inhibitor | Preclinical | CD123 ADC with a topoisomerase-I payload. CD123 is validated with a DNA-alkylating ADC (pivekimab-sunirine) and a toxin fusion (tagraxofusp), and the topoisomerase-I class is validated on many solid-tumour antigens (trastuzumab-deruxtecan). No corpus ADC pairs CD123 with a topoisomerase-I payload. CD123 is on leukaemic stem cells and internalises (pivekimab-sunirine, tagraxofusp); a topoisomerase-I payload would be less potent than the IGN alkylator and might widen the window against normal progenitors, at the cost of activity in quiescent stem cells.Caveat: Quiescent leukaemic stem cells are the therapeutic goal of CD123 targeting, and topoisomerase-I poisons act mainly on replicating cells; this construct may treat bulk disease but miss the stem cell pool.Proposed by OnCo open pipeline, searched 2026-09-23. | Untried | |
| 65 | CD20 | Topoisomerase I inhibitor | No public evidence | CD20 ADC with a topoisomerase-I payload. CD20 is the most validated B-cell antigen in the corpus across naked antibodies (rituximab, obinutuzumab), a radioconjugate (ibritumomab-tiuxetan) and four T-cell engagers (epcoritamab, glofitamab), yet no ADC. Topoisomerase-I payloads with acid-labile linkers release drug in the tumour microenvironment (sacituzumab-govitecan), which is the mechanism a non-internalising antigen would rely on. CD20 barely internalises, which is why no CD20 ADC exists despite four approved CD20 antibodies; a permeable topoisomerase-I payload released extracellularly (as sacituzumab-govitecan partly is) is the only route that makes sense, and it would be a delivery experiment as much as a drug.Caveat: The whole proposal rests on extracellular payload release working at therapeutic levels; if it does not, CD20's lack of internalisation kills the idea, as it has for tubulin payloads.Proposed by OnCo open pipeline, searched 2026-09-23. | Untried | |
| 65 | CD33 | DNA crosslinker (PBD dimer) | Clinical evidence | CD33 ADC with a PBD dimer payload. CD33 is validated with a calicheamicin ADC (gemtuzumab-ozogamicin) and PBD dimers are validated on CD19 (zynlonta). The corpus has no CD33 PBD conjugate; a lower-DAR PBD could address the calicheamicin resistance driven by drug efflux in AML blasts. CD33 internalises and is myeloid-restricted, but it sits on normal myeloid progenitors, so any potent DNA-damaging payload will cause deep, prolonged cytopenias; the earlier CD33 PBD programme was stopped for that reason.Caveat: A CD33 PBD ADC would need a way round the myelosuppression that stopped the earlier attempt, for example as a bridge to transplant rather than a stand-alone therapy.Proposed by OnCo open pipeline, searched 2026-09-23. | Untried | |
| 65 | GPRC5D | Topoisomerase I inhibitor | No public evidence | GPRC5D ADC with a topoisomerase-I payload. GPRC5D is validated by an approved T-cell engager (talquetamab) and a phase-3 CAR-T (arlocabtagene-autoleucel), and the topoisomerase-I payload class is validated on many antigens (trastuzumab-deruxtecan). No corpus product delivers a cytotoxic payload to GPRC5D, which would give patients who have exhausted BCMA and CD3-engaging therapies an off-the-shelf option. GPRC5D is an orphan GPCR restricted to plasma cells and keratinised tissue (talquetamab); a payload delivered by an antibody would spare T-cell engagement toxicities but the receptor's internalisation rate is not established and myeloma proliferates slowly.Caveat: GPRC5D is expressed in hair follicles, nails and tongue; an ADC would carry the same skin, nail and dysgeusia toxicity as talquetamab, and antigen loss after talquetamab is documented.Proposed by OnCo open pipeline, searched 2026-09-23. | Untried | |
| 63 | CD38 | Topoisomerase I inhibitor | No public evidence | CD38 ADC with a topoisomerase-I payload. CD38 is validated by two approved antibodies (daratumumab, isatuximab) and the corpus holds a CD38 ADC with a tubulin payload in phase 2 (sti-6129), but no CD38 topoisomerase-I ADC. Topoisomerase-I payloads are the best-validated ADC class (trastuzumab-deruxtecan, sacituzumab-govitecan) and could act on daratumumab-refractory disease that still expresses the antigen. CD38 is expressed at high density on myeloma cells and internalises slowly, which suits a permeable payload with bystander killing; the antigen is also on NK cells and red-cell precursors, so haematological toxicity is the expected limit.Caveat: Most relapsed myeloma patients have received daratumumab, which down-regulates CD38 for months; the ADC would need antigen to remain, and the low proliferation of myeloma cells may blunt a replication-dependent payload.Proposed by OnCo open pipeline, searched 2026-09-23. | Untried | |
| 60 | GD2 (disialoganglioside) | Topoisomerase I inhibitor | No public evidence | GD2 (disialoganglioside) ADC with a topoisomerase-I payload. GD2 is validated by two approved antibodies in neuroblastoma (dinutuximab, naxitamab) and topoisomerase-I payloads are the best-validated ADC class (trastuzumab-deruxtecan); the corpus has no GD2 ADC of any payload class. Children with relapsed neuroblastoma receive irinotecan and temozolomide as standard, so a GD2-directed camptothecin would concentrate a drug already known to be active. GD2 is a glycolipid, not a protein, and internalises poorly; its expression on peripheral nerves causes the pain of dinutuximab, which a cytotoxic payload could worsen. A bystander-capable payload released near the cell is the only plausible design.Caveat: Poor internalisation of a glycolipid antigen and on-nerve expression are two serious objections; preclinical proof that payload reaches tumour without nerve toxicity is needed before any child is dosed.Proposed by OnCo open pipeline, searched 2026-09-23. | Untried |
Not placed
15 of 93 medicines in this format (16%)These medicines belong to the format but their target is on no record the engine reads: the targets field is empty, the target lists no such drug, the trials linked to it name no target of its own, and the modality, mechanism and summary text name none the corpus knows. They are listed here rather than placed by guesswork; adding the target to the record puts them in the grid on the next build.
How this grid is read from the records
Each medicine's parts come from its own record: the targets field first, else the target records that list the medicine, else a sibling conjugate that shares its antibody name, else the trials linked to it, else the target names the corpus knows found in its modality, mechanism or summary text. Payloads come from the ADC payload registry, the payload field, or the INN stem of the name (deruxtecan is DXd, vedotin is MMAE, tesirine is a PBD dimer); the linker type from the linker registry or field; the DAR from the payload field where it is written. Every part carries the fields it was read from and a confidence in the JSON file.
What the states mean, and do not
Approved: a medicine in the cell has an approval row or a regulator's approved entry and is not recorded as withdrawn. In development: a recruiting, active or planned trial, a development-phase record status, or active studies in the ClinicalTrials.gov index, and no approval. Tried and stopped: every medicine in the cell is withdrawn, negative or historic, or its only trial evidence is a terminated, withdrawn or negative study, or its approval was withdrawn. Untried: no medicine in this corpus combines the two parts.
A cell is coloured by its strongest medicine; the table shows each medicine with its own state. The reasons quoted under Stopped, and why are the records' words, including the registry's whyStopped text where the sponsor wrote one, and include stopped studies of medicines that are still in development elsewhere. Nothing here is medical advice.