(S,S,S)-VH032-cyclopropane-F-C4-aldehyde is an E3 ligase ligand-linker conjugate used in the synthesis of PROTAC cis-VZ185.

I-BET151 (GSK1210151A) is a novel selective BET inhibitor for BRD2, BRD3 and BRD4 with IC50 of 0.5 μM, 0.25 μM, and 0.79 μM, respectively.

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.

Pomalidomide-C2-NH2 hydrochloride is a synthesized E3 ligase ligand-linker conjugate that incorporates the Pomalidomide based cereblon ligand and a linker used in PROTAC technology.

An E3 ligase ligand-linker conjugate for PROTAC..

TL13-12 is a novel Anaplastic Lymphoma Kinase (ALK)-PROTAC developed through conjugation of TAE684 and the cereblon ligand pomalidomide.

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.

N-piperidine Ibrutinib hydrochloride (Compound 1) is a reversible Ibrutinib derivative. N-piperidine Ibrutinib hydrochloride is a potent BTK inhibitor with IC50s of 51.0 and 30.7 nM for WT BTK and C481S BTK, respectively. N-piperidine Ibrutinib hydrochloride can be used as a BTK ligand in the synthesis of a series of PROTACs, such as SJF620. SJF620 is a potent PROTAC BTK degrader with a DC50 of 7.9 nM.

Pomalidomide 4'-alkylC5-acid is a synthesized E3 ligase ligand-linker conjugate that incorporates the Pomalidomide based cereblon ligand and a PEG linker used in PROTAC technology.

Pomalidomide-PEG3-azide is a synthesized E3 ligase ligand-linker conjugate that incorporates the Pomalidomide based cereblon ligand and 3-unit PEG linker used in PROTAC technology.

PROTAC-O4I2 is a PROTAC targets splicing factor 3B1 (SF3B1). PROTAC-O4I2 induces FLAG-SF3B1 degradation with an IC50 value of 0.244 μM in K562 cells. PROTAC-O4I2 also induces cellular apoptosis in K562 WT cells.

Thalidomide-O-C4-COOH is a synthesized E3 ligase ligand-linker conjugate that incorporates the Thalidomide based cereblon ligand and a linker used in PROTAC technology.

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).

Thalidomide-5-CH2-NH2 (hydrochloride) is the Thalidomide-based cereblon ligand used in the recruitment of CRBN protein. Thalidomide-5-CH2-NH2 (hydrochloride) can be connected to the ligand for protein by a linker to form PROTACs.

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.

YW-N-7 (TFA) is a PROTAC that targets both the inhibition and degradation of RET kinase, with a DC50 of 88 nM. YW-N-7 (TFA) exhibits antitumor activity in a KIF5B-RET-driven xenograft mouse tumor model and can be used in the area of cancer.

YN14-H is a PROTAC degrader targeting KRASG12C. YN14-H inhibits cell growth in NCI-H358 and MIA PaCa-2 cells (IC50 values of 0.042, 0.021 μM, DC50 values of 28.9, 18.1 nM, respectively). YN14-H significantly induces apoptosis and inhibits migration. YN14-H demonstrates favorable pharmacokinetic properties and excellent antitumor activity in vivo.

TYD-68 is a highly efficient and selective CRBN-recruited TYK2 PROTAC degrader with a DC50 value of 0.42 nM. TYD-68 significantly inhibits IL-12 and IFN-α-induced STAT4 and STAT1 phosphorylation, thereby blocking TYK2-dependent signaling pathways. TYD-68 can be used in the study of psoriasis.

TrimTAC1 is a PROTAC degrader that selectively targets the degradation of the multimeric protein Nucleoporin.

TO-1187 is a selective HDAC6 PROTAC degrader (DC50: 5.81 nM). TO-1187 promotes the ubiquitination and degradation of HDAC6 and can be used in the study of hematological malignancies and solid tumors.

Tamoxifen-PEG-Clozapine is an estrogen receptor α (ERα) PROTAC degrader. Tamoxifen-PEG-Clozapine degrades ERα via a ubiquitin-proteasome system that uses the ubiquitin protein ligase E3 component N-recognin 5. Tamoxifen-PEG-Clozapine can be used for the research of cancer.

SMD-1087 is a PROTAC that selectively targets SMARCA2 (DC50=8 nM, Dmax=89%) and SMARCA4 with a DC50 of 1 μM.

SJ44236 is the PROTAC degrader for BET that degrades BRD2 (DC50 = 0.127 nM), BRD3 and BRD4. SJ44236 exhibits cytotoxicity in cell MV4-11 and HD-MB03 with IC50s of 0.12 nM and 0.92 nM. SJ44236 downregulates the expression of c-Myc, upregulates the expression of p53. SJ44236 exhibits a good orally bioavailability of 45% in mice.

SD-2301 is a PROTAC based STAT3 degrader (Red: STAT3 inhibitor.

RP03707 is a PROTAC based KRASG12D degrader (Red: KRASG12D inhibitor and may cause cross-immunoreactivity with anti-Forskolin antibodies.

RNAse L RIBOTAC (compound C64) is an RNA-degrading chimera which binds to a four-way RNA helix called SL5 in the 5’ UTR of the SARS-CoV-2 RNA genome and inhibits the virus replication in lung epithelial carcinoma cells.

RJS308 is the PROTAC degrader for cyclosporin A (CypA) with a DC50 of 284 nM. RJS308 exhibits antiviral activcity through inhibition of HIV-1 and HCV replication.

RD-23 is an orally active and selective RET PROTAC degrader. RD-23 promotes ubiquitination and degradation of RETG810C mutation, with a DC50 value of 11.7 nM. RD-23 inhibits the activation of downstream Shc signaling and induces Apoptosis. RD-23 can be used for the research of RET-related cancers.