Metastatic Prostate Cancer

Sorafenib (Bay 43-9006) is a potent oral active multikinase inhibitor. Sorafenib blocks autophosphorylation and activity of receptor tyrosine kinases (VEGFR-2, VEGFR-3) and RAF family kinases, thereby suppressing the RAF/MEK/ERK and PI3K/Akt pathways, inhibiting STAT3 phosphorylation, and selectively inhibiting the MAPK pathway in cancer cells. Sorafenib induces cell cycle arrest, autophagy, apoptosis, and PARP cleavage, reduces Bcl-2, Bcl-XL, cyclin D1 levels, and activates Bak and Bax. Sorafenib inhibits tumor growth and metastasis in mouse and rat models. Sorafenib can be used for cancer research, such as colon, breast, non-small-cell lung cancer (NSCLC), ovarian, pancreatic, melanoma, colorectal and hepatocellular carcinoma.

Abemaciclib (LY2835219) is a selective and BBB-permeable CDK4/6 inhibitor with IC₅₀ values of 2 nM and 10 nM for CDK4 and CDK6, respectively.

Inobrodib (CCS1477) is an orally active, potent, and selective inhibitor of the p300/CBP bromodomain. Inobrodib binds to p300 and CBP with K_d values of 1.3 and 1.7 nM, respectively, and with 170/130-fold selectivity compared with BRD4 with a K_d of 222 nM. CCS1477 inhibits cell proliferation in prostate cancer cell lines and decreases androgen receptor (AR)- and C-MYC-regulated gene expression.

Acalabrutinib (ACP-196) is an orally active, irreversible, and highly selective second-generation BTK inhibitor. Acalabrutinib binds covalently to Cys481 in the ATP-binding pocket of BTK. Acalabrutinib demonstrates potent on-target effects and efficacy in mouse models of chronic lymphocytic leukemia (CLL). Acalabrutinib can be used for CLL research. Acalabrutinib is a click chemistry reagent, itcontains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.

Itraconazole (R51211) is a triazole antifungal agent and a potent and orally active Hedgehog (Hh) signaling pathway antagonist with an IC₅₀ of ~800 nM. Itraconazole potently inhibits lanosterol 14α-demethylase (cytochrome P450 enzyme), thereby inhibits the oxidative conversion of lanosterol to ergosterol. Itraconazole has anticancer and antiangiogenic effects. Itraconazole is a oxysterol-binding protein (OSBP) inhibitor.

Darolutamide (ODM-201) is an orally active competitive androgen receptor (AR) antagonist. Darolutamide has a K_i of 11 nM for rat wild-type AR (wtAR) and IC₅₀ of 26 nM for human wild-type AR (hAR)-mediated transcriptional activation. Darolutamide inhibits testosterone-induced AR nuclear translocation and transcriptional activation. Darolutamide exerts selective effects on AR-positive cells by inhibiting AR-dependent signaling pathways, and its active metabolite retains full antagonistic activity against AR mutants. Darolutamide can be used for the research of prostate cancer, including androgen receptor-dependent prostate cancer.

BMX ligand-1 (Compound 9) is a BMX ligand. BMX ligand-1 serves as a target protein ligand for the synthesis of BMX PROTAC degraders, such as IHMT-BMX-068 (HY-184005). BMX ligand-1 is applicable to prostate cancer research.

Trioxifene (LY133314 free base) is an orally active and selective estrogen receptor (ER) modulator with human ERα IC₅₀ of 203.49 nM and K_i of 20.84 nM. Trioxifene binds estradiol receptors, inhibits ERα-mediated gene expression, reduces circulating gonadotrophin levels. Trioxifene can be used for the research of advanced breast cancer and androgen-independent, metastatic prostatic adenocarcinoma.

Apalutamide (ARN-509) is a potent and competitive androgen receptor (AR) antagonist, binding AR with an IC₅₀ of 16 nM.

Sorafenib-d₃ (Donafenib) is the deuterated-labeled Sorafenib (HY-10201). Sorafenib (Bay 43-9006) is a potent oral active multikinase inhibitor. Sorafenib blocks autophosphorylation and activity of receptor tyrosine kinases (VEGFR-2, VEGFR-3) and RAF family kinases, thereby suppressing the RAF/MEK/ERK and PI3K/Akt pathways, inhibiting STAT3 phosphorylation, and selectively inhibiting the MAPK pathway in cancer cells. Sorafenib induces cell cycle arrest, autophagy, apoptosis, and PARP cleavage, reduces Bcl-2, Bcl-XL, cyclin D1 levels, and activates Bak and Bax. Sorafenib inhibits tumor growth and metastasis in mouse and rat models. Sorafenib can be used for cancer research, such as colon, breast, non-small-cell lung cancer (NSCLC), ovarian, pancreatic, melanoma, colorectal and hepatocellular carcinoma.

Risedronic acid (Risedronate) is a bisphosphonate and potent antiresorptive agent. Risedronic acid induces Apoptosis. Risedronic acid inhibits the transfer of farnesyl pyrophosphate groups to parasite proteins. Risedronic acid inhibits osteoclast-mediated bone resorption and alters bone metabolism. Risedronic acid inhibits blood-stage Plasmodium falciparum (IC₅₀ of 20.3 μM).

YS5 (FOR 46/FG-3246 antibody) is an anti-CD46 antibody. YS5 can serve as an ADC Antibody to synthesize the ADC FOR 46/FG-3246. YS5 is applicable to research related to metastatic castration-resistant prostate cancer.

Rilotumumab (AMG 102) is an anti-HGF (anti-hepatocyte growth factor) monoclonal antibody, inhibits HGF/MET-driven signaling. Rilotumumab shows anti-tumor activity, and can be used in castration-resistant prostate cancer (CRPC) and solid tumor research.

Sorafenib (Standard) (Bay 43-9006 (Standard)) is the analytical standard of Sorafenib (HY-10201). This product is intended for research and analytical applications. Sorafenib (Bay 43-9006) is a potent oral active multikinase inhibitor. Sorafenib blocks autophosphorylation and activity of receptor tyrosine kinases (VEGFR-2, VEGFR-3) and RAF family kinases, thereby suppressing the RAF/MEK/ERK and PI3K/Akt pathways, inhibiting STAT3 phosphorylation, and selectively inhibiting the MAPK pathway in cancer cells. Sorafenib induces cell cycle arrest, autophagy, apoptosis, and PARP cleavage, reduces Bcl-2, Bcl-XL, cyclin D1 levels, and activates Bak and Bax. Sorafenib inhibits tumor growth and metastasis in mouse and rat models. Sorafenib can be used for cancer research, such as colon, breast, non-small-cell lung cancer (NSCLC), ovarian, pancreatic, melanoma, colorectal and hepatocellular carcinoma.

ZEN-3694 (BET-IN-19) is an orally active BET inhibitor. ZEN-3694 regulates the function of BET proteins, thereby downregulating pathways involved in cell cycle regulation, ER signaling, AR signaling, AR splice variants, MYC, GR, cell growth, inflammation, and cellular immune responses. ZEN-3694 inhibits proliferation, induces apoptosis, reverses the upregulation of CDK6 and CCND1, restores cell cycle arrest, and inhibits CDK6 via miR-34a-5p. ZEN-3694 can be used in research related to HER2 breast cancer and metastatic castration-resistant prostate cancer.

MS181 is a BMI1 and RING1B degrader with antiproliferative activity. MS181 induces degradation via an EED-, CRBN-, and ubiquitin-proteosome system-dependent pathway, with preferential targeting over PRC2 components. MS181 acts in VHL-defective cancer cells. MS181 serves as a chemical biology tool to study PRC1 roles in cancer. MS181 can be used for the research of myelogenous leukemia, renal cell carcinoma, metastatic prostate cancer, triple negative breast cancer.

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.

Sorafenib-¹³C,d₃ (Bay 43-9006-¹³C,d₃) is the ¹³C, deuterated-labeled Sorafenib (HY-10201). Sorafenib (Bay 43-9006) is a potent oral active multikinase inhibitor. Sorafenib blocks autophosphorylation and activity of receptor tyrosine kinases (VEGFR-2, VEGFR-3) and RAF family kinases, thereby suppressing the RAF/MEK/ERK and PI3K/Akt pathways, inhibiting STAT3 phosphorylation, and selectively inhibiting the MAPK pathway in cancer cells. Sorafenib induces cell cycle arrest, autophagy, apoptosis, and PARP cleavage, reduces Bcl-2, Bcl-XL, cyclin D1 levels, and activates Bak and Bax. Sorafenib inhibits tumor growth and metastasis in mouse and rat models. Sorafenib can be used for cancer research, such as colon, breast, non-small-cell lung cancer (NSCLC), ovarian, pancreatic, melanoma, colorectal and hepatocellular carcinoma.

MIP-1095 TFA (RPS-001 TFA) is a PSMA inhibitor with a K_i value of 0.24 nM. MIP-1095 TFA binds to PSMA with high affinity and can be internalized into PSMA-expressing cancer cells. When radiolabeled with ¹²³I, ¹²⁴I or ¹³¹I, MIP-1095 TFA enables SPECT/CT imaging, PET/CT imaging or targeted radiation delivery, respectively. ¹³¹I-MIP-1095 TFA can alter serum PSA levels and relieve bone pain. MIP-1095 TFA can be used in research related to metastatic castration-resistant prostate cancer.

Sorafenib-d4 (Bay 43-9006-d4) is the deuterated-labeled Sorafenib (HY-10201). Sorafenib (Bay 43-9006) is a potent oral active multikinase inhibitor. Sorafenib blocks autophosphorylation and activity of receptor tyrosine kinases (VEGFR-2, VEGFR-3) and RAF family kinases, thereby suppressing the RAF/MEK/ERK and PI3K/Akt pathways, inhibiting STAT3 phosphorylation, and selectively inhibiting the MAPK pathway in cancer cells. Sorafenib induces cell cycle arrest, autophagy, apoptosis, and PARP cleavage, reduces Bcl-2, Bcl-XL, cyclin D1 levels, and activates Bak and Bax. Sorafenib inhibits tumor growth and metastasis in mouse and rat models. Sorafenib can be used for cancer research, such as colon, breast, non-small-cell lung cancer (NSCLC), ovarian, pancreatic, melanoma, colorectal and hepatocellular carcinoma.