BRD4 Degrader

PROTAC BRD4 Degrader-20 (Compound 195) is a PROTAC degrader that targets BRD4 for degradation by recruiting VHL. PROTAC BRD4 Degrader-20 is applicable to the research of diffuse large B-cell lymphoma.

YT117R is a PROTAC degrader targeting BRD4. YT117R binds stereoselectively and site-specifically to the cysteine residue C1113 of DCAF1 to form a covalent interaction. YT117R promotes BRD4 degradation via a DCAF1-dependent, proteasome- and cullin-RING E3 ligase-mediated process. YT117R exhibits stereoselective activity dependent on wild-type DCAF1, which is blocked by the DCAF1^C1113A mutation.

PROTAC BRD4 Degrader-18 is a PROTAC BRD4 degrader. PROTAC BRD4 Degrader-18 binds to BRD4 and recruits E3 ubiquitin ligase, inducing ubiquitination and proteasomal degradation of BRD4. PROTAC BRD4 Degrader-18 exhibits antiproliferative activity against ovarian cancer cell lines. PROTAC BRD4 Degrader-18 can be used in research related to ovarian cancer.

PROTAC BRD4 Degrader-6 (compound 32a) is a potent small-molecule BRD4PROTAC degrader with IC₅₀ value of 2.7 nM for BRD4 BD1. PROTAC BRD4 Degrader-6 potently degrades BRD4 protein and inhibits the expression of c-Myc. PROTAC BRD4 Degrader-6 inhibits the proliferation of pancreatic cancer cell line BxPC3 and induces apoptosis. PROTAC BRD4 Degrader-6 can be used for human pancreatic cancer research.

PROTAC BET Degrader-17 is a potent BET protein PROTAC degrader. By recruiting the VHL E3 ligase, PROTAC BET Degrader-17 specifically degrades BRD2, BRD3 (DC₅₀=0.09 nM) and BRD4 (IC₅₀=4.3 nM). PROTAC BET Degrader-17 exhibits strong anti-tumor activity in acute myeloid leukemia (AML) studies; it not only inhibits cancer cell proliferation, induces cell cycle arrest and apoptosis, but also effectively suppresses tumor growth in xenograft mouse models. PROTAC BET Degrader-17 can be used to explore targeted therapies for acute myeloid leukemia.

PROTAC BRD4 Degrader-16 is a BRD4 PROTAC degrader. PROTAC BRD4 Degrader-16 induces sustained degradation of both long and short isoforms of BRD4 in cancer cells, causes cell cycle arrest, and exhibits only extremely low apoptosis effects. PROTAC BRD4 Degrader-16 can be used in studies related to acute myeloid leukemia.

PROTAC BRD4 Degrader-23 is a visible light-regulated BRD4 PROTAC degrader, with DC₅₀ values of 6871 nM and < 30 nM in the dark and under light exposure, respectively; its IC₅₀ values are 1172 nM and 140 nM under the corresponding conditions. PROTAC BRD4 Degrader-23 shows inhibited activity in dark environments, and recovers BRD4 degradation ability upon irradiation with 405 nm visible light. PROTAC BRD4 Degrader-23 inhibits tumor cell proliferation in a visible light-dependent manner. PROTAC BRD4 Degrader-23 can be used in studies of BRD4-dependent B-cell lymphoma.

PROTAC BRD4 Degrader-28 is a PROTAC degrader targeting BRD4, with a DC₅₀ of 5.4 nM for BRD4 in HEK293 cells. PROTAC BRD4 Degrader-28 binds to the CRBN E3 ubiquitin ligase, forms a ternary complex with BRD4, and thereby mediates the ubiquitination and proteasomal degradation of BRD4. PROTAC BRD4 Degrader-28 can be used in cancer research.

PROTAC BRD4 Degrader-27 is a selective cereblon-mediated BRD4 PROTAC degrader. PROTAC BRD4 Degrader-27 exhibits anticancer activity, induces G1 phase arrest, and inhibits DNA synthesis and colony formation. PROTAC BRD4 Degrader-27 suppresses HCC1806 tumor growth in xenograft mouse models. PROTAC BRD4 Degrader-27 can be used in breast cancer-related research.

PROTAC BRD4 Degrader-50 is a BRD4 PROTAC degrader with a DC₅₀ of 11.4 nM (HEK293). PROTAC BRD4 Degrader-50 induces BRD4 degradation via the proteasome and CRBN. PROTAC BRD4 Degrader-50 is applicable to cancer research.

PROTAC BRD4 Degrader-47 is a heterobifunctional PROTAC that selectively degrades BRD4 in a SYVN1-dependent manner, with a DC₅₀ of 0.93 μM. PROTAC BRD4 Degrader-47 can be used in cancer-related research such as breast cancer.

MM-02-08 is a BRD4 PROTAC degrader with a DC₅₀ of approximately 10 nM. MM-02-08 mediates mono-ubiquitination and poly-ubiquitination modifications of target proteins without impairing cell viability. MM-02-08 is applicable to related research on triple-negative breast cancer, prostate cancer, and other diseases.

PROTAC BRD2 BD1 Degrader-1 is a potent and selective BRD2 BD1 PROTAC degrader, with a DC₅₀ of 65 nM, an EC₅₀ of 423 nM, and a K_d of 69 nM against BRD2 BD1. PROTAC BRD2 BD1 Degrader-1 induces the formation of a ternary complex between the BET bromodomain and the VHL E3 ubiquitin ligase complex, triggering VCB-dependent degradation of the target bromodomain. PROTAC BRD2 BD1 Degrader-1 can be used in cancer research.

PROTAC BET Degrader-16 (Compound A10) is a BET PROTAC degrader with a DC₅₀ of 0.31 nM against BRD4, and it preferentially targets BRD4 over other BET family members. PROTAC BET Degrader-16 degrades BRD2, BRD3 and BRD4 via the ubiquitin-proteasome system, a process that requires target binding and recruitment of the CRBN E3 ligase. PROTAC BET Degrader-16 induces cell cycle arrest and promotes apoptosis. PROTAC BET Degrader-16 exerts anti-tumor activity against acute myeloid leukemia.

JV8 is a BRD4 PROTAC degrader with a target K_d of 0.65 μM. JV8 preferentially induces BRD4 degradation in the cytoplasm via the ubiquitin-proteasome system. JV8 exhibits dose-dependent and time-dependent BRD4 degradation activity and is capable of inducing cell apoptosis. JV8 inhibits tumor growth in a dose-dependent manner and induces BRD4 degradation in tumor tissues in vivo. JV8 can be used in research related to various cancers such as breast cancer and pancreatic cancer.

TMU454 is an ASGPR-targeting GalNAc-PROTAC BRD4 degrader conjugate. TMU454 undergoes ASGPR-mediated endocytosis and CTSB cleavage to release MZ1, which selectively degrades BRD4 in ASGPR-positive hepatocellular carcinoma cells via the VHL/UPS/proteasome pathway. TMU454 inhibits cancer cell proliferation and colony formation, and suppresses tumor growth in vivo. TMU454 can be used for research related to hepatocellular carcinoma.

PROTAC BET Degrader-15 is a BET PROTAC degrader with DC₅₀ values of <0.10 nM, <0.01 nM, and <0.01 nM against BRD2, BRD3, and BRD4, respectively. PROTAC BET Degrader-15 induces significant G2/M phase cell cycle arrest and triggers apoptosis. PROTAC BET Degrader-15 causes marked downregulation of c-Myc, accompanied by upregulation of the cell cycle inhibitory protein p21, downregulation of CDK6, and an increase in the apoptosis marker cleaved PARP. PROTAC BET Degrader-15 is applicable to the research of hematologic malignancies and lung cancer.

PROTAC BRD4 Degrader-3 is a potent BRD4 PROTAC degrader with DC₅₀ values ​​of 164 nM and 80 nM at 4 h and 24 h, respectively. PROTAC BRD4 Degrader-3 induces the ubiquitination and subsequent proteasomal degradation of BRD4 by recruiting the ubiquitin E3 ligase KLHDC2. PROTAC BRD4 Degrader-3 can be used in breast cancer research.

GXF-111 is a BRD3 and BRD4-L PROTAC degrader. Its BD1 and BD2 Ki values against human BRD3 are 11.97 nM and 2.45 nM, respectively. The degradation activity of GXF-111 depends on its binding to BET proteins and Cereblon, as well as the involvement of a functional proteasome. The degradation selectivity of GXF-111 is mainly determined by differences in degradation kinetics and cell types. GXF-111 induces G₁ phase cell cycle arrest, downregulates c-Myc expression, upregulates p21 expression, and exhibits antiproliferative activity against a variety of cancer cell lines. GXF-111 can serve as a research tool for cancer-related studies.

JY-21 is a BRD4 PROTAC degrader active against both long and short BRD4 isoforms. JY-21 binds to TRIM28, RACK1, LMO7 and FUS to induce proteasomal degradation of BRD4 isoforms (DC₅₀: 5.944 μM for long BRD4 isoform; 3.797 μM for short BRD4 isoform). JY-21 is applicable to research related to triple-negative breast cancer.