Ask about this productRelated genes to: KLK2 Blocking Peptide
- Gene:
- KLK2 NIH gene
- Name:
- kallikrein related peptidase 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1988-08-11
- Date modifiied:
- 2015-11-13
Related products to: KLK2 Blocking Peptide
Related articles to: KLK2 Blocking Peptide
- Prognostic biomarker panels identified through bulk sequencing approaches have shown utility in localized prostate cancer but are limited by underlying molecular heterogeneity. Spatial transcriptomics offers a complementary approach to investigate spatial gene expression patterns and the tissue- and cell-type-associated localization of their constituent biomarker genes. - Source: PubMed
Publication date: 2026/03/30
Taylor Kristofer GJohannessen BjarneMills Ian GRye Morten BAxcrona KarolSkotheim Rolf I - KLK2 is an androgen-regulated gene critical in prostate cancer biology with multiple KLK2-targeted therapies in clinical development. We investigated KLK2 RNA expression patterns and associations with molecular features to provide context for emerging KLK2-targeted treatments. - Source: PubMed
Publication date: 2026/03/12
McKay Rana RNazari Shayan SElliott AndrewSmith NormBarata PedroKilari DeepakGarje RohanHaffner Michael CMorrissey ColmRupnow Brent ABasu SubhasreeDrake CharlesRose BrentBagrodia AdityaAgarwal NeerajAntonarakis Emmanuel SBeltran Himisha - Liver receptor homolog-1 (LRH-1) is a key regulator in multiple cancers, including prostate cancer, making its antagonists a promising therapeutic strategy. However, the development of potent LRH-1 antagonists remains largely inadequate, underscoring an urgent unmet need for novel candidates with therapeutic potential. Herein, we report the discovery and characterization of a novel class of indole-based LRH-1 antagonists. Starting from high-throughput virtual screening, we employed structure-based drug design strategy to optimize lead compounds, yielding 26 (XY25026) and 28 (XY25028), which exhibit potent LRH-1inhibition with IC values of 280 nM and 300 nM, respectively. In cellular assays, 26 and 28 inhibited the cell proliferation across a panel of androgen receptor (AR)-positive prostate cancer cell lines with distinct androgen responsiveness and AR signaling profiles and suppressed AR target genes (KLK2 and KLK3). Importantly, oral administration of 26 and 28 elicited significant in vivo antitumor efficacy in a 22Rv1 xenograft model, with no detectable systemic toxicity observed in treated mice. These results identify 26 and 28 as promising orally bioavailable LRH-1 antagonists, validating them as attractive lead molecules for further structural optimization and development for castration-resistant prostate cancer (CRPC) therapy. - Source: PubMed
Publication date: 2026/02/16
Ma KaiyuanJin WeiqinZhang YanLu ZhifangZhuang XiaoxiLi JunhuaJing XinyiWang JunLi LiangZhou YananLi XinXu TingtingXu JinxinMa JinmingDeng JunjieZhai XinLin BinXu YongShen Hui - Most therapy options for castration-resistant prostate cancer (CRPCa) target the androgen axis. Human kallikrein-related peptidase (KLK) 2, a serine protease, is a downstream target gene of the androgen receptor (AR) involved in cancer progression, but also known to have an AR-independent function. Tissue KLKs, especially KLK2, are promising targets for therapy in advanced PCa because of their high PCa specificity and their correlation to the rising cancer grade and stage. By inhibition with the recombinant protease inhibitor MDPK67b targeting KLK2 and other trypsin-like KLKs including KLK4 and KLK14, we investigated the antitumor response and the influence on AR downstream target genes with MDPK67b in PCa cell lines in vitro. - Source: PubMed
Publication date: 2026/01/11
Lehner FabienneSalemi SouzanMillan ChristopherKündig ChristophEberli Daniel - Dysregulation of extracellular matrix (ECM) degradation pathways has been increasingly implicated in major depressive disorder (MDD), yet its genetic basis remains unclear. This study investigated the relationship between ECM-related genetic polymorphisms and MDD susceptibility. In a case-control study, we analyzed 317 MDD patients and 1268 sexmatched controls from the Taiwan Biobank (TWB). Genomic DNA was analyzed using the Affymetrix TWB array, targeting single nucleotide polymorphisms (SNPs) in 140 ECM degradation genes (Reactome database). Full-model association tests identified significant SNPs, validated with 5000 max(T) permutations and adjusted via logistic regression for age, body mass index, education level, and marital status. We identified 12 SNPs across 10 ECMrelated genes significantly associated with MDD, including ADAM metallopeptidase domain 17 (, rs55820761), brevican (, rs11264511), CD44 molecule (, rs12270356), collagen type XVII alpha 1 chain (; rs2282436 and rs10883962), collagen type III alpha 1 chain (; rs16830979 and rs10883962), collagen type VI alpha 6 chain (, rs16830219), cathepsin L (, rs2274611), Kallikrein-related peptidase 2 (, rs2664156), matrix metallopeptidase 11 (, rs738791), and nicastrin (, rs3753391). This study provides the first genetic evidence linking ECM degradation pathways to MDD susceptibility, identifying novel biomarkers for early diagnosis and precision therapy. Further research and cross-population studies are needed to confirm these findings. - Source: PubMed
Publication date: 2025/12/01
Zailani HalliruChen Daniel Tzu-LiLin Sheng-CheLee Jia-HauLi Mei-LingChang Jane Pei-ChenSu Kuan-Pin