FLT3/JAK2/BRD4 ligand-1 is a FLT3/JAK2/BRD4 ligand. FLT3/JAK2/BRD4 ligand-1 can be used for synthesis PROTAC FLT3/JAK2/BRD4 Degrader-1.

SHP2 ligand-3 is a PROTAC target protein ligand that can be used to synthesize SHP2 protein degrader-1.

ER ligand-12 is an estrogen receptor (ER) ligand that can be used in the synthesis of PROTACs, such as PROTAC ER Degrader-2.

PROTAC Her3-binding moiety 2 is a Her3 inhibitor. PROTAC Her3-binding moiety 2 can be used for synthesis of PROTAC Her3 Degrader-8.

Androgen receptor ligand 3 is an androgen receptor (AR) ligand. Androgen receptor ligand 3 is linked to an IAP ligand via a linker to form an ERα PROTAC degrader.

SARS-CoV-2 Mpro ligand 1 (Compound S15) is a PROTAC target protein ligand. SARS-CoV-2 Mpro ligand 1 can be used to synthesize BP-198.

HPK1 ligand 3 is a ligand for target protein for PROTAC that can be used to synthesize PROTAC HPK1 Degrader-4.

WZH-15-125 is a potent ALK inhibitor. WZH-15-125 can effectively overcome drug resistance, especially compound ALK mutations. WZH-15-125 has an IC50 of 101.7 nM for the highly refractory G1202R/L1196M mutation that is resistant to Lorlatinib. WZH-15-125 can be used as a PROTAC target protein ligand to synthesize PROTAC WZH-17-002. WZH-15-125 can be used in the research of non-small cell lung cancer.

ARCC-4 is a low-nanomolar androgen receptor (AR) degrader based on PROTAC, with a DC50 of 5?nM. ARCC-4 is an enzalutamide-based von Hippel-Lindau (VHL)-recruiting AR PROTAC and outperforms enzalutamide. ARCC-4 effectively degrades clinically relevant AR mutants associated with antiandrogen therapy.

dBET57 is a novel BRD4 heterobifunctional small-molecule ligand (PROTAC), exhibits significant and selective degradation of BRD4 BD1 (DC50/5h=500 nM), but is inactive on BRD4 BD2..

dBET6 is a highly potent, selective and cell-permeable degrader of BET with an IC50 of 14 nM, and has antitumor activity.

MS 177 (MS-177) is a potent and selective EZH2 degarder (PROTAC) based on EZH2 inhibitor C24 with CRBN ligand pomalidomide with DC50 of 0.2 uM in EOL-1 cells.MS177 effectively degraded cellular EZH2-PRC2, suppressed global H3K27me3 in leukaemia cells.MS177 exhibited half-maximal degradation concentration (DC50) values of 0.2 ± 0.1 μM and 1.5 ± 0.2 μM, and maximum degradation (Dmax) values of 82% and 68%, respectively, in EOL-1 and MV4;11 cells.MS177 efficiently suppresses EZH2-PRC2 functions, also efficiently induces Myc degradation in cancer cells, suppresses EZH2-PRC2 functions.MS177 efficiently induces leukaemia cell growth inhibition, apoptosis and cell cycle progression arrest, which is more effective than EZH2 inhibitors. MS177 (i.p. injection, 50-1 g/kg) represses AML growth without apparent toxicity in PDX models.

XY028-140 (MS-140) is a potent and selective PROTAC-based CDK4/CDK6 kinase degrader. XY028-140 specifically inhibits RB-E2F signaling and reduces CDK4 and CDK6 protein levels in a dose- and time-dependent manner in vitro. In addition, XY028-140 can degrade its targets by linking them with ubiquitin-proteasome mechanism. Further, the degradation of CDK4/6 protein by XY028-140 is specifically mediated by CRBN. Therefore, XY028-140 effectively and selectively inhibits and degrades CDK4/6 kinase by targeting CDK4/6 kinase in CDK4/6i-S (CDK4/6 inhibitor-sensitive) tumor cells to the CRL4-CRBN-E3 ubiquitin complex. Compared with CDK6 wild-type cells, XY028-140 treatment of cells expressing wild-type or mutation-activated CDK6 resulted in a more effective degradation of CDK6 (S178P).

KH103 is a highly potent, catalytically-driven glucocorticoid receptor (GR) PROTAC degrader, demonstrate excellent performance in passively preventing ligand-induced gene expression activation in the absence of partial agonistic transcriptional triggering and crosstalk inhibition. KH 103 efficiently degrades glucocorticoid receptor (GR) in vitro and in vivo. In HEK293 cells, KH-103 (1 µM) induced rapid and nearly complete GR degradation within one hour. This degradation was highly potent, with significant depletion observed at 10 nM and near-complete depletion at 100 nM. KH-103 demonstrated effective and ​​reversible​​ GR degradation across diverse in vitro models from multiple tissues and species.Mechanistically, KH-103 promoted GR nuclear translocation but did not activate GR-mediated gene transcription and exhibited no nonspecific transcriptional effects alone. Furthermore, KH-103 effectively blocked dexamethasone (DEX)-induced GR signaling, demonstrating greater potency than comparator inhibitors.Critically, KH-103 also effectively depleted GR protein in the mouse pituitary gland in vivo and modulated corticosterone levels, confirming pharmacological activity beyond cell-based systems.

Abd110 (compound 42i) is a PROTAC molecule derived from lenalidomide that specifically targets ATR kinase for degradation. This compound demonstrates remarkable selectivity, effectively reducing both ATR and phospho-ATR levels while sparing related DNA damage response kinases ATM and DNA-PKcs.

MS8847 represents a novel PROTAC molecule that selectively targets EZH2 for degradation by recruiting the VHL E3 ubiquitin ligase complex. This compound mediates potent, proteasome-dependent elimination of EZH2, demonstrating significant anti-proliferative effects against both AML and TNBC cell lines.

THAL-SNS-032 is a novel CDK9 degrader PROTAC consisting of a CDK-binding SNS-032 ligand linked to a thalidomide derivative that binds the E3 ubiquitin ligase Cereblon (CRBN).

HJM-561 is a potent, selective and orally bioavailable EGFR PROTAC degrader, selectively degrades the EGFR C797S-containing triple mutants Del19/T790M/C797S and L858R/T790M/C797S with DC50 values of 9.2 nM and 5.8 nM, respectively.

KT-253 is a potent small molecule that stabilizes p53 while simultaneously acting as a PROTAC to degrade MDM2 (DC50 = 0.4 nM). It demonstrates strong antiproliferative effects in RS4;11 leukemia cells (IC50 = 0.3 nM), inducing G2/M cell cycle arrest and apoptosis. In vivo studies confirm its antitumor activity in mouse models.

KT-333 is a first-in-class molecular glue that induces ​selective degradation of STAT3 via the ubiquitin-proteasome system by simultaneously engaging ​STAT3 and the VHL E3 ligase. This novel mechanism enables potent ​STAT3 depletion with minimal off-target effects, demonstrating strong ​anti-tumor activity in hematologic malignancies.

BTK-IN-29 (compound 14) is an inhibitor of Btk.

PROTAC BRD4 Degrader-21 (Compound 74) is a potent and selective degrader of BRD4, demonstrating robust tumor growth suppression in mouse xenograft models. Its efficacy supports its potential as a promising candidate for anticancer drug development.

SD-436 is a highly potent and selective STAT3 degrader with DC50 of 0.1 nM in human PBMCs and displays >10,000-fold degradation selectivity for STAT3 over other STAT proteins.

SD-36 (STAT3 degrader SD-36) is a potent, selective STAT3 degrader (PROTAC), potently induces the degradation of STAT3 protein in vitro and in vivo.SD-36 is designed using an analogue of CRBN ligand lenalidomide and the STAT3 inhibitor SI-109, binds to recombinant STAT3 protein with Ki of 11 nM.SD-36 (250 nM) depleted >90% of STAT3 protein in MOLM-16 cells after 4 hr treatment and >50% of STAT3 protein in DEL, KI-JK and SU-DHL-1 cells after 7 hr treatment, also efficiently degraded STAT3 protein in murine cells.SD-36 displays extremely high cellular selectivity for degradation of STAT3 over other STATs.SD-36 effectively degrades both wild-type and mutated STAT3 proteins in cells, effectively degrades mutated STAT3 (D661Y, K658R mutant), also effectively degrades CRISPR-mutated homozygous Y705F mutant STAT3 protein in DLD-1/STAT3Y705F/Y705F cells.SD-36 displayed strong growth-inhibitory activities in a subset of leukemia and lymphoma cell lines (MOLM-16 cell line IC50, 35 nM), 100-fold more potent than SI-109.SD-36 (i.v. 25 mg/kg) effectively and selectively depletes STAT3 protein, achieves complete and long-lasting tumor regression in in mouse xenograft tumors.

KT-474 is a highly active and selective, orally bioavailable IRAK4 degrader being developed for the treatment of toll-like receptor (TLR)/interleukin-1 receptor (IL-1R)-driven immune-inflammatory diseases.

NX-2127 is a potent, selective, and orally bioavailable BTK degrader with Kd of 18 nM (for WT BTK), 45 nM (BTK C481S), 18 nM (BTK T474I), 44 nM (BTK M437R), 97 nM (BTK V416L), and 88 nM (BTK L528W), respectively. NX-2127 efficiently engages the intracellular ubiquitin-proteasome system to simultaneously bind both BTK and the CRBN E3 ubiquitin ligase complex, inducing polyubiquitination and proteasome-dependent degradation of BTK, IKZF1, and IKZF3.

ARV-110 is an orally active, specific androgen receptor (AR) PROTAC degrader. ARV-110 promotes ubiquitination and degradation of AR. ARV-110 can be used for the research of prostate cancer.

ARV471 is an orally bioavailable estrogen receptor-targeting (ER-targeting) PROTAC for the treatment of patients with locally advanced or metastatic ER+/HER2- breast cancer.

YJ1206 is an orally bioavailable PROTAC compound that selectively degrades CDK12 and CDK13, demonstrating potent activity (IC50 = 12.55 nM) in VCaP cells. It induces DNA damage, triggers apoptosis, and drives tumor regression in treatment-resistant prostate cancer PDX models, highlighting its therapeutic potential.

endo-BCN-O-PNB is an alkyl/ether-based PROTAC linker that can be used in the synthesis of PROTACs.