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A relative of PSA that stays attached to prostate cancer cells, used as a T-cell engager address by J&J.
Human kallikrein-2 (KLK2) is an androgen-regulated serine protease that activates PSA; unlike PSA it is retained on the prostate cell membrane, which makes it a usable address for cell-surface therapies. Expression is nearly universal in prostate cancer and prostate-restricted elsewhere, so a KLK2-directed drug can engage T cells against the tumour with little on-target damage to other tissues. The lead agent is Johnson & Johnson's pasritamig (JNJ-78278343, a KLK2 x CD3 bispecific), which showed low cytokine release and PSA responses in phase 1 and is in phase 3 (KLK2-P3-01) in metastatic castration-resistant prostate cancer. Open questions are whether KLK2 expression persists in neuroendocrine or AR-independent disease and how it compares with PSMA as an engager target. The plain version: KLK2 is a cousin of PSA that stays stuck to cancer cells, so drugs can grab it.
In plain words · A relative of PSA that stays attached to prostate cancer cells, used as a T-cell engager address by J&J.
A relative of PSA that stays attached to prostate cancer cells, used as a T-cell engager address by J&J.
Serine protease activating PSA; androgen-regulated.
1 product aims at KLK2 (kallikrein-2): bispecific antibodies. Because it sits on the outside of the cell, it can be reached from the bloodstream: antibodies flag the cell, ADCs deliver a toxin, radioligands deliver radiation, and CAR-T or bispecifics bring a T cell.
Tumour-associated overexpression: 1 cell-killing or cell-finding medicine (Pasritamig) aim at the antigen, which HPA finds stained high in 1 normal tissue; the medicine relies on the tumour carrying more of it than the normal tissue it shares it with. HPA KLK2: RNA tissue enriched (prostate 531 nTPM); high antibody staining in 1 normal tissue; highest cancer staining prostate cancer (8 of 10 high). Distribution: 1 cancer family in the corpus carries a prevalence row, label threshold or catalogue link for it (Prostate cancer); Open Targets associates it with 0 specific cancer types at or above 0.5. (Rule 5 of scripts/fetch-target-specificity.ts.)
Sources: Human Protein Atlas KLK2 tissue; Human Protein Atlas KLK2 pathology; Open Targets ENSG00000167751 associations
First described 1987. Earliest sequence paper UniProt cites for the protein: Schedlich L.J. et al, DNA, 1987, "Primary structure of a human glandular kallikrein gene". Source.
Serine protease activating PSA; androgen-regulated.
RNA: tissue enriched (prostate 531 nTPM), detected in some normal tissues.
RNA cancer enriched: Prostate Adenocarcinoma 752 pTPM.
Human Protein Atlas version 25.1, antibody staining at reliability approved, enhanced or supported; used under CC BY-SA 3.0. Staining counts are patients per level in the atlas cohort, not population prevalence.
Pasritamig is Johnson & Johnson's bispecific T-cell engager that binds KLK2 on prostate cancer cells and CD3 on T cells, with a deliberately low-affinity CD3 arm. In phase 1 about 40% of patients had a PSA50 response with far less cytokine release syndrome than other engagers, and a phase 3 trial began in 2025.
Query for this target: (TITLE:"KLK2" OR ABSTRACT:"KLK2" OR TITLE:"kallikrein-2" OR ABSTRACT:"kallikrein-2") 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 KLK2 (kallikrein-2), not a curated reading list.
Shares Prostate cancer and the tag t-cell-engager-target.
Shares Pasritamig and the tag t-cell-engager-target.
Shares Prostate cancer and the tag t-cell-engager-target.
Shares Pasritamig, Prostate cancer.