Mezigdomide (CC-92480) is a potent, novel, selective and active cereblon E3 ubiquitin ligase modulator (CELMoD) that often acts as a molecular glue. Mezigdomide has antimyeloma activity.

dCeMM3 (2-(1H-benzimidazol-2-ylsulfanyl)-N-(5-chloropyridin-2-yl)acetamide) is a glue degrader. dCeMM3 prompts an interaction of CDK12-cyclin K with a CRL4B ligase complex, result in inducing ubiquitination and degradation of cyclin K.

WBC100 (14-D-Valine-TPL) is a potent, selective, and orally active c-Myc glue degrader that targets the ubiquitin E3 ligase CHIP-mediated 26S proteasome pathway, primarily utilized in research for c-Myc overexpressing tumors [1].

KB02-SLF is a PROTAC-based nuclear FKBP12 degrader, known as a molecular glue. It facilitates the degradation of nuclear FKBP12 by covalently modifying DCAF16, an E3 ligase. Moreover, KB02-SLF enhances the longevity of protein degradation in biological systems. The compound SLF acts as a linker, binding to the ubiquitin E3 ligase ligand KB02, resulting in the formation of KB02-SLF[1].

N-Boc-4-pentyne-1-amine is an alkyl chain-based PROTAC linker compound utilized in the synthesis of PROTAC MG-277[1].

Naphthyridine carbamate dimer (NCD) acts as a molecular glue for DNA, facilitating specific structural alterations within targeted functional DNA sequences to modulate their activity [1].

Lenalidomide (sodium), a Thalidomide derivative, serves as a molecular glue and an orally active immunomodulator. It acts as a cereblon (CRBN) ligand and triggers selective ubiquitination and subsequent degradation of the lymphoid transcription factors IKZF1 and IKZF3 via the CRBN-CRL4 ubiquitin ligase. Echoing its specificity, Lenalidomide (sodium) inhibits the proliferation of mature B-cell lymphomas, notably multiple myeloma, and promotes IL-2 secretion from T cells [1] [2].

MG-277 is a molecular glue compound transformed from PROTAC degradation agent, MG-277 potently inhibits tumor cell growth in a p53-independent manner.

LSN3160440 is an allosteric modulator of GLP-1R, functioning as a protein-protein interaction (PPI) stabilizer or molecular glue. It aids in the binding of inactive GLP-1 (9-36) NH2 to GLP-1R, enhancing receptor activation and potential therapeutic effects [1] [2].

(R)-CR8 trihydrochloride (CR8, (R)-Isomer trihydrochloride) is a CDK1/2/5/7/9 inhibitor that acts as a molecular glue degrader with neuroprotective activity and induces apoptosis.

Lenalidomide hydrochloride (CC-5013 hydrochloride), a Thalidomide derivative, functions as molecular glue and serves as an orally active immunomodulator. As a ligand for the ubiquitin E3 ligase cereblon (CRBN), it facilitates the selective ubiquitination and degradation of the lymphoid transcription factors IKZF1 and IKZF3 through the CRBN-CRL4 ubiquitin ligase. Specifically, Lenalidomide hydrochloride inhibits the growth of mature B-cell lymphomas, including multiple myeloma, and promotes IL-2 release from T cells [1] [2].

Antitumor agent-100 hydrochloride (compound A6), serving as both an apoptosis inducer and molecular glue, exhibits superior anti-tumor activity [1].

GBD-9, a dual-mechanism degrader, effectively promotes the degradation of BTK and GSPT1 through recruitment of E3 ligase cereblon (CRBN). As a PROTAC molecule, GBD-9 induces BTK degradation, while also acting as a molecular glue for GSPT1 degradation, demonstrating potent inhibition of cancer cell growth [1].

KB02-JQ1 is a potent and specific proteolysis targeting chimera (PROTAC) that specifically degrades BRD4, acting as a molecular glue. It does not degrade BRD2 or BRD3. The mechanism of action involves covalent modification of the E3 ligase DCAF16, thereby promoting BRD4 degradation. Importantly, KB02-JQ1 demonstrates enhanced stability and durability in facilitating protein degradation within biological systems. The compound forms a complex with the ubiquitin E3 ligase ligand KB02 through a linker, resulting in the formation of KB02-JQ1[1].

HQ461 is a molecular gel that promotes CDK12-DDB1 interactions and triggers cyclin K degradation, which impairs CDK12 function, leading to decreased CDK12 substrate phosphorylation, downregulation of DNA damage response genes, and cell death.

dCeMM2 is a glue degrader. dCeMM2 prompts an interaction of CDK12-cyclin K with a CRL4B ligase complex, leading to the ubiquitination and degradation of cyclin K.

dCeMM1 is a RBM39 glue degrader. dCeMM1 can re-direct the activity of the CRL4DCAF15 ligase. dCeMM1 can decrease the expression levels of RBM39 in WT KBM7 cells.

dCeMM4 (Compound 5) is a glue degrader that induces cyclin K ubiquitination and degradation through prompting an interaction of CDK12-cyclin K with a CRL4B ligase complex [1].