2. Disease Areas
  3. Cancer Urogenital Disease
  4. Prostate Cancer Urogenital Cancer
  5. Castration-Resistant Prostate Cancer

Castration-Resistant Prostate Cancer

Castration-resistant prostate cancer (CRPC) is a progressive, noncurable form of prostate cancer that continues to grow despite castrate levels of testosterone, typically marked by rising prostate-specific antigen (PSA) levels. It is driven by persistent androgen receptor (AR) signaling, even in low-androgen environments, often through intracrine androgen synthesis from adrenal precursors like dehydroepiandrosterone (DHEA). Metastatic CRPC (mCRPC) remains a major therapeutic challenge, though calcitriol—the active metabolite of vitamin D—has demonstrated anti-tumor effects in preclinical models via induction of cell cycle arrest, apoptosis, differentiation, and inhibition of angiogenesis and metastasis. These effects are mediated by the vitamin D receptor (VDR), which interacts with AR signaling pathways; notably, androgens suppress CYP24A1 (a calcitriol-degrading enzyme), while vitamin D promotes androgen inactivation through induction of metabolic enzymes like CYP3A4 and SULT2B1b. However, these protective mechanisms are disrupted in advanced disease, where CYP24A1 is overexpressed and CYP3A4/SULT2B1b are downregulated. Emerging evidence supports the potential of safe-dose vitamin D3 supplementation in slowing low-grade prostate cancer progression, and future strategies may involve combining next-generation calcitriol analogs with CYP24A1 inhibitors or agents targeting cancer stem cells, such as sulforaphane, to enhance therapeutic efficacy.

Castration-Resistant Prostate Cancer (26):

Cat. No. Product Name CAS No. Purity Chemical Structure
  • HY-P990688
    Xaluritamig 2559056-68-5 ≥99%
    Xaluritamig (AMG-509) is a bispecific T cell engager and cytolytic agent with a Kd of 27.6 nM for human CD3ε. Xaluritamig binds to CD3ε via an anti-CD3 single-chain variable fragment (scFv) domain, and to STEAP1 via a bispecific anti-STEAP1 antigen-binding fragment (Fab) domain, thereby recruiting and activating T cells and forming a bridge between T cells and STEAP1-expressing cancer cells. Xaluritamig induces T cell-mediated redirected cytotoxicity, tumor cell lysis, cytokine release, CD8+ T cell activation and expansion, as well as tumor stasis or regression. Xaluritamig contains an Fc domain with no effector function, which prolongs serum half-life, exhibits only minimal activity against cells with low STEAP1 expression and normal cells, and shows extremely low target-related off-tumor toxicity in cynomolgus monkeys. Xaluritamig is used in STEAP1×CD3 XmAb 2+1 immunotherapy and in research on metastatic castration-resistant prostate cancer and Ewing sarcoma.
    Xaluritamig
  • HY-P990673
    Vandortuzumab 99.00%
    Vandortuzumab (DSTP-3086S Antibody; RG-7450 Antibody) is a humanized anti-STEAP1 IgG1 antibody and antimitotic agent that can be conjugated with MMAE (HY-15162) to form the antibody-drug conjugate (ADC) Vandortuzumab vedotin. Vandortuzumab vedotin specifically binds to STEAP1 and drives internalization of the complex, releasing the MMAE (HY-15162) payload intracellularly. After binding to tubulin, MMAE inhibits cell division and induces cell death. Vandortuzumab exhibits antitumor activity in preclinical xenograft models of prostate cancer and can be used for research related to metastatic castration-resistant prostate cancer (mCRPC).
    Vandortuzumab
  • HY-P991015
    Pasritamig 2921676-04-0 99.031%
    Pasritamig (JNJ-78278343; KLCB-245) is a bispecific T-cell engager (BiTE) that targets the complex of human kallikrein KLK2 and CD3 receptor. Pasritamig redirects the cytotoxicity of T cells to KLK2-expressing tumor cells and induces T cell-mediated lysis of KLK2-expressing prostate cancer cells. Administered via subcutaneous injection, subcutaneous infusion or intravenous infusion, Pasritamig exhibits antitumor activity against metastatic castration-resistant prostate cancer. Pasritamig has a safety profile with an extremely low incidence of cytokine release syndrome and can be safely administered in an outpatient setting. Pasritamig is applicable to the research of metastatic castration-resistant prostate cancer.
    Pasritamig
  • HY-N5074
    Terrestrosin D 179464-23-4 99.30%
    Terrestrosin D is an orally active apoptosis inducer. Terrestrosin D induces cell cycle arrest at the G1 and S phases, reduces mitochondrial membrane potential, and inhibits the growth of cancer cells and endothelial cells. Terrestrosin D is studied in castration-resistant prostate cancer and pulmonary fibrosis.
    Terrestrosin D
  • HY-P9992
    Pelgifatamab 2414550-93-7 99.884%
    Peligifatamab is a PSMA-targeted α-radioimmunoconjugate with an EC50 of 1.2 nM against human targets. Peligifatamab induces DNA damage, DNA double-strand breaks, cell cycle arrest and apoptosis (Apoptosis) in PSMA-positive prostate cancer cells. Peligifatamab reduces cell viability in a manner dependent on cellular PSMA expression levels. Peligifatamab inhibits tumor growth and tumor-induced abnormal bone growth in prostate cancer bone metastasis models. Peligifatamab exhibits antitumor efficacy in subcutaneous prostate cancer models and xenograft models. Peligifatamab can be used for the research of metastatic castration-resistant prostate cancer.
    Pelgifatamab
  • HY-184124
    JZY3032
    JYZ3032 is an orally active super inhibitor of androgen receptor (AR) and p300/CBP. JYZ3032 redirects the catalytic activity of p300 and locks the complex in a transcriptionally inactive state, thereby inhibiting AR-driven transcription and proliferation. JYZ3032 induces deep and durable tumor regression in castration-resistant and patient-derived xenograft models, and exhibits good tolerability. JYZ3032 can be used in research related to metastatic castration-resistant prostate cancer and prostate cancer.
    JZY3032
  • HY-P99528
    Vandortuzumab vedotin 1471985-92-8 99.52%
    Vandortuzumab vedotin (DSTP 3086S; RG 7450) is a STEAP1-targeted antibody-drug conjugate (ADC). Vandortuzumab vedotin binds specifically to STEAP1, triggers internalization of the conjugate complex, mediates intracellular release of monomethyl auristatin E, inhibits cell division, and induces cell death. Vandortuzumab vedotin exhibits antitumor activity in preclinical prostate cancer xenografts. Vandortuzumab vedotin can be used for the research of metastatic castration-resistant prostate cancer.
    Vandortuzumab vedotin
  • HY-183667
    JNJ-pan-AR 1332390-06-3
    JNJ-pan-AR is an orally active androgen receptor (AR) inhibitor with an IC50 of 19 nM and a Ki of 8.4 nM against human wild-type AR. JNJ-pan-AR abolishes androgen-induced KLK2 and KLK3 mRNA expression and reduces androgen-dependent colony formation in prostate cancer cells. JNJ-pan-AR blocks AR nuclear translocation, inhibits PSA protein expression, and represses the growth of AR-dependent tumor cells and ARF877L-driven tumor xenografts. JNJ-pan-AR blocks transactivation and signaling of wild-type AR and various mutant AR variants. JNJ-pan-AR is applicable for research on castration-resistant prostate cancer.
    JNJ-pan-AR
  • HY-170329
    PROTAC AR Degrader-8 3044108-04-2 99.98%
    PROTAC AR Degrader-8 is the PROTAC degrader for androgen receptor (AR) that degrades AR-FL with DC50s of 0.018 μM and 0.14 μM in 22Rv1 cell and LNCaP cell, degrades AR-V7 with DC50 of 0.026 μM in 22Rv1 cell. PROTAC AR Degrader-8 inhibits the proliferation of cancer cell 22Rv1 and LNCaP with IC50 values of 0.038 μM and 1.11 μM. PROTAC AR Degrader-8 arrests cell cycle at G2/M phase, induces apoptosis in 22Rv1 cell. PROTAC AR Degrader-8 exhibits anticancer efficacy in mouse and zebrafish model. PROTAC AR Degrader-8 can be used for the research of prostate cancer, castration-resistant prostate cancer.
    PROTAC AR Degrader-8
  • HY-19337
    Ketodarolutamide 1297537-33-7 98.72%
    Ketodarolutamide (ORM-15341) is a potent, high-affinity nonsteroidal competitive full antagonist of androgen receptor (AR). Ketodarolutamide displays a Ki value of 8 nM for rat wild-type AR and an IC50 value of 38 nM in AR-HEK293 cells. Ketodarolutamide inhibits testosterone-induced nuclear translocation of the AR and antagonizes both overexpressed and mutant ARs. Ketodarolutamide specifically suppresses the proliferation of AR-dependent prostate cancer cells and exhibits antitumor activity in models of castration-resistant prostate cancer (CRPC) . Ketodarolutamide is suitable for the mechanistic and therapeutic research of prostate cancer.
    Ketodarolutamide
  • HY-134635
    Dehydrozingerone 1080-12-2 99.98%
    Dehydrozingerone is a ginger-derived component and cyclin D1 inhibitor that downregulates cyclin D1 expression and induces cell cycle G1 phase arrest. Dehydrozingerone reduces the proliferative capacity of castration-resistant prostate cancer cells under in vitro conditions. Dehydrozingerone reduces subcutaneous tumor growth by inhibiting cell proliferation and angiogenesis. Dehydrozingerone exerts antibacterial and antifungal activities via its α,β-unsaturated carbonyl conjugated system. Dehydrozingerone can be used in studies related to castration-resistant prostate cancer, bacterial infections, and food spoilage fungal infections.
    Dehydrozingerone
  • HY-45661
    Inixaciclib 2370913-42-9 99.93%
    Inixaciclib (NUV-422) is a blood-brain barrier-penetrant inhibitor of CDK2, CDK4 and CDK6. Inixaciclib inhibits cancer cell growth. Inixaciclib induces anti-tumor activity in xenograft models of glioblastoma, CDK4/CDK6 inhibitor-resistant HR+ HER2- metastatic breast cancer, and anti-androgen-resistant prostate cancer. Inixaciclib can be used for the research of relapsed or metastatic castration-resistant prostate cancer.
    Inixaciclib
  • HY-W414731
    N-(3-Methylphenyl)anthranilic acid 16524-22-4 99.82%
    N-(3-Methylphenyl)anthranilic acid is an aldo-keto reductase 1C3 (AKR1C3)and AKR1C2 inhibitor with IC50 values of 0.24 μM and 0.38 μM, respectively. N-(3-Methylphenyl)anthranilic acid shows no inhibition of COX-1 or COX-2. N-(3-Methylphenyl)anthranilic acid can be used for the research of castration resistant prostate cancer.
    N-(3-Methylphenyl)anthranilic acid
  • HY-141546
    Pocenbrodib 2304372-79-8 98.49%
    Pocenbrodib is a P300/CBP inhibitor. Pocenbrodib blocks the function of P300/CBP and inhibits the acetylation of histones and non-histone proteins. Pocenbrodib may be used in research related to castration-resistant prostate cancer and other cancers.
    Pocenbrodib
  • HY-170820
    XYD049 3006788-11-7 99.46%
    XYD049 is a CRBN-based molecular glue degrader targeting GSPT1, with a DC50 of 19 nM. XYD049 mediates the formation of a ternary complex between CRBN and GSPT1, thereby triggering CRBN- and proteasome-dependent degradation of GSPT1. By degrading GSPT1, XYD049 downregulates castration-resistant prostate cancer (CRPC)-related oncogenes, including BCL2, CDK2, E2F3, EGFR, HSP90B1, TMPRSS2, AR, AR-V7, PSA and c-Myc. XYD049 inhibits cancer cell growth and suppresses tumor growth in mice. XYD049 can be used for research on castration-resistant prostate cancer. XYD049 consists of a linker (black part) NH2-C5-NH-Boc (HY-W004710), a CRBN-based E3 ligase ligand (blue part) Thalidomide 4-fluoride (HY-41547), and a target protein ligand (red part) GSPT1 ligand-1 (HY-170821), among which the E3 ligase ligand plus linker forms the conjugate E3 Ligase Ligand-linker Conjugate 158 (HY-170822).
    XYD049
  • HY-16247
    Apoptone 183387-50-0
    Apoptone (HE3235) is an orally active 3β-androstanediol analog. Apoptone reduces the expression of androgen receptor (Androgen receptor) and decreases intratumoral androgen levels. Apoptone exhibits anticancer activity against castration-resistant prostate cancer.
    Apoptone
  • HY-P10740
    CBP-1018 2923068-30-6 99.21%
    CBP-1018 is a PDC (peptide-drug conjugate) formed by conjugating Monomethyl auristatin E (HY-15162) to a dual-targeting ligand of FLOR1/PSMA (prostate-specific membrane antigen) via a linker (HY-78738). CBP-1018 binds to FLOR1 and prostate-specific membrane antigen (PSMA). CBP-1018 is applicable to the research of solid tumors and metastatic castration-resistant prostate cancer.
    CBP-1018
  • HY-183632
    QW-5-70
    QW-5-70 is a potent colchicine‑site tubulin inhibitor that blocks tubulin polymerization. QW-5-70 induces mitotic and G2/M cell cycle arrest, triggers mitochondrial apoptosis, and suppresses cancer cell colony formation and migration. QW-5-70 overcomes P‑glycoprotein‑mediated multidrug resistance and inhibits drug‑resistant tumor growth. QW-5-70 demonstrates strong in vitro and in vivo antitumor efficacy in neuroblastoma and prostate cancer models. QW-5-70 can be used for the research of high-risk neuroblastoma and castration-resistant prostate cancer.
    QW-5-70
  • HY-183273
    BRD4/AKT-IN-1 3087270-50-3
    BRD4/AKT-IN-1 is a BRD4/AKT inhibitor with BRD4 IC50 66.12 nM and AKT1 IC50 143.81 nM. BRD4/AKT-IN-1 blocks BRD4-mediated c-Myc transcriptional regulation, modulates AKT1 signaling, decouples AKT phosphorylation from pro-survival effectors. BRD4/AKT-IN-1 induces G0/G1 cell cycle arrest via downregulated phosphorylated RB, cyclin E1, CDK2. BRD4/AKT-IN-1 elevates LC3B levels to promote autophagy. BRD4/AKT-IN-1 promotes apoptosis in cancer cells. BRD4/AKT-IN-1 can be used for the research of metastatic castration-resistant prostate cancer.
    BRD4/AKT-IN-1
  • HY-181727
    AR/AR-V7 degrader-1
    AR/AR-V7 degrader-1 is an orally active AR and AR-V7 degrader. AR/AR-V7 degrader-1 disrupts the interaction between AR/AR-V7 and HSP90, leading to their ubiquitination and degradation in castration-resistant prostate cancer cells. AR/AR-V7 degrader-1 regulates the expression of cell cycle-related proteins in prostate cancer cells (downregulates CDK4, CDK6, Cyclin D1, Cyclin E1; upregulates P21) and induces G0/G1 phase arrest. AR/AR-V7 degrader-1 inhibits the proliferation and migration of prostate cancer cells. AR/AR-V7 degrader-1 suppresses the growth of castration-resistant prostate cancer tumors in nude mice and induces the degradation of AR and AR-V7 in tumor tissues. AR/AR-V7 degrader-1 is applicable to the research of castration-resistant prostate cancer.
    AR/AR-V7 degrader-1