Mal-VC-PAB-DMEA-PNU-159682 is a agent-linker conjugate for ADC with potent antitumor activity by using the anti-topoisomerase II agent, PNU-159682, linked via the lysosomally cleavable dipeptide, Mc-VC-PAB. Mal-VC-PAB-DMEA-PNU-159682 can be used in the synthesis of Anti-CD22-NMS249, which is an bivalent AR (Androgen Receptor) degrader. ATC-324 can reduce nuclear AR levels and downregulate target gene expression of AR and AR-v7, and also has a degradation effect on common AR mutants in PCa.

Mal-Val-Ala-amide-(3)PEA-PNU-159682 is a Drug-Linker Conjugates for ADC, composes of ADC linker (Mal-Val-Ala-amide-(3)PEA) and ADC cytotoxin PNU-159682. Dorrigocin A can inhibit the carboxymethyltransferase involved in Ras processing and reverse the morphology of ras-transformed NIH/3T3 cells. Dorrigocin A is promising for research of anti-cancer and anti-arthritis agents.

Mal-PNU-159682 is a Drug-Linker Conjugates for ADC, composes of ADC linker (maleimide) and ADC cytotoxin PNU-159682, which is a synthetic derivative of prostaglandin F2α.

Mal-PEG4-Val-Cit-PAB-MMAE is part of a drug-linker conjugate for ADC. Mal-PEG4-Val-Cit-PAB-MMAE contains a degradable ADC linker Mal-PEG4-Val-Cit-PAB and a potent tubulin inhibitor MMAE.

Mal-N(Me)-C6-N(Me)-PNU-159682 (Compound 27), an agent-linker conjugate for ADC, consists the ADC linker Mal-N(Me)-C6-N(Me) and a potent ADC cytotoxin PNU-159682. Mal-N(Me)-C6-N(Me)-PNU-159682 (Compound 27) selectively delivers the payload to CD46-expressing cells, where the linker is cleaved by cathepsin B to release PNU-159682, inducing DNA damage and apoptosis. Mal-N(Me)-C6-N(Me)-PNU-159682 shows durable tumor regression in xenograft (PDX) models of non-small cell lung cancer (NSCLC) and colorectal cancer (CRC).

Mal-L-Dap(Boc)-Osu is an ADC Linker, and can be used for synthesis of ADCs.

Mal-amide-PEG8-Val-Cit-PAB-PNP is a cleavable ADC linker featuring a maleimide, a PEG spacer, a Val-Cit dipeptide, a PAB. and a PNP carbonate. Maleimide is a thiol-specific covalent linker which is used to label cysteine residues in proteins while the PNP group acts as a highly activated leaving group. Val-Cit linkers are cleaved by cytoplasmic peptidases.

Mal-amide-PEG8-Val-Cit-PAB-OH is a cleavable ADC linker featuring a maleimide, a hydrophilic PEG spacer, a Val-Cit dipeptide, and a PAB functional group. Maleimide is used to covalently bind free thiols on the cysteine residues of proteins. The Val-Cit dipeptide is cleaved by cellular proteases within the cell to allow for efficient payload delivery with the help of the PAB structure.

M3686 (Compound 29) is a potent, selective TEAD1 inhibitor with an IC50 value of 51 nM. M3686 also shows weaker binding activity on TEAD3. M3686 potently inhibits cell viability against YAP-dependent NCI-H226 cell line with an IC50 value of 0.06 uM. M3686 shows strong anti-tumor effects in the NCI-H226 xenograft model.

LZ9 is a ATP-competitive CDK1 and CDK2 inhibitor. LZ9 has the potential for the research of colorectal cancer (CRC).

LZ-007 is an agonist for farnesoid X receptor (FXR) with an EC50 of 51 nM measuring by TR-FRET assay, or an EC50 of 76 nM in HepG2 cell. LZ-007 exhibits good pharmacokinetic characheristics in SD rats. LZ-007 ameliorates western diet and CCl4-induced mice metabolic dysfunction-associated steatohepatitis

LysoPalloT-NH-amide-C3-ph-m-O-C11 is an agonist for GPR174 with an EC50 of 34 nM.

LXQ-87 is an oral noncompetitive inhibitor of PTP1B with an IC50 of 1.061 μM, showing hypoglycemic activity. LXQ-87 alleviates insulin resistance and promotes cellular glucose uptake, making it useful for research on type 2 diabetes.

LT-188A is a potent TGR5 agonist with an EC50 of 23 μM. LT-188A decreases the levels of inflammatory mediators in macrophages.

Lonitoclax is a B-cell lymphoma 2 (Bcl-2) inhibitor. Lonitoclax has comparable anti-tumor efficacy to Venetoclax.

LON 954, a tremorogenic agent, is a reversible monoamine oxidase (MAO) inhibitor. LON 954 inhibits MAO activity in various tissue preparations.

LO-4-25 is a covalent degrader targeting the androgen receptor (AR) and its truncated variant AR-V7. LO-4-25 covalently binds to the E3 ubiquitin ligase CUL4 DCAF16, promoting the ubiquitination of AR and AR-V7, which subsequently are recognized and degraded by the proteasome, reducing the protein levels of AR and AR-V7 in cells. LO-4-25 is promising for research of androgen-independent prostate cancers.

LNK4-S is a drug-linker conjugate, that can be used for synthesis of ADC molecule M-VA-EXA and F-VA-EXA.

LIB3S0280 is a potent TBK1 inhibitor with an IC50 value of 493.9 nM. LIB3S0280 can inhibit TBK1 downstream signaling by decreasing the phosphorylation of IκBα and AKT. LIB3S0280 leads to G2/M arrest and induces apoptosis in pancreatic cancer cells. LIB3S0280 shows significant inhibition against pancreatic cancer cell lines that highly express TBK1 with IC50 values of 6.64-10.98 μM at 96 h. LIB3S0280 has the potential for pancreatic ductal adenocarcinoma (PDAC) research.

LH168 is a potent and selective chemical probe for WDR5, with a SPR Kd value of 13 nM.

LH10 is a fexaramine-based agonist for FXR with an EC50 of 0.14 μM. LH10 exhibits liver protection efficacy, ameliorates the alpha naphthylisothiocyanate (ANIT)-induced cholestasis, APAP. Benzoyl coenzyme A (sodium) is A derivative of Coenzyme A (CoA) in which the mercaptan group of CoA binds to the benzoyl group. Benzoyl coenzyme A (sodium) is involved in the catalytic reaction as a substrate for the acyl transfer reaction. Benzoyl coenzyme A (sodium) is a versatile metabolic intermediate that can be used to reveal substrate specificity of enzymes, metabolic regulation, and drug metabolism.

Leucomycin A4 is a macrolide antibiotic that can be extracted from S. kitasatoensis. Leucomycin A4 inhibits a variety of bacteria, including S. aureus, B. subtilis, C. diphtheriae, N. gonorrhoeae, and H. influenzae (MICs = 0.15, 1.25, 0.15, 0.6, and 0.15 µg/ml, respectively).

Leucinostatin H is a polypeptide antibiotic discovered in Paecilomyces marquandii, characterized by a tertiary amine-oxide terminal group. Leucinostatin H exhibits inhibitory activity against Gram-positive bacteria, such as Bacillus subtilis, B. cereus, and Staphylococcus aureus (MIC 10-100 μg/mL). Leucinostatin H holds potential for research in anti-infective and plant disease control applications.

Lenalidomide-hex-5-ynoic acid is a conjugate of E3 ligase ligand and linker, and can be used to synthesize PROTACs, such as PROTAC cGAS degrader-1.

Lenalidomide-Glycolic acid is a E3 Ligase Ligand-Linker Conjugate for PROTAC-class FLT3 degrader LWY713.

Lenalidomide-C13-piperazine-Boc is a conjugate of the E3 ligase ligand and the linker, that can be used for synthesis of PROTAC degrader NC-R17.

Lenalidomide-amide-pimelic acid is an E3 ligase ligand-linker conjugate that incorporates the Lenalidomide based CRBN ligand and Linker. Lenalidomide-amide-pimelic acid can be used for synthesis of PROTAC MNK1 degrader-1.

Lenalidomide-5-Br-amide-C2-Br is an E3 ligase ligand-linker conjugate. Lenalidomide-5-Br-amide-C2-Br can be used to synthesize PROTAC DDR1 degrader-1. Palbociclib is an orally active selective CDK4 and CDK6 inhibitor with IC50 values of 11 and 16 nM, respectively.

LC-SF-14 is a selective dual inhibitor of SHP2 and FGFR (IC50 values are 71.6 and 8.9 nM, respectively). LC-SF-14 inhibits FGFR2-FRS2α-SHP2-MAPK signaling and ERK phosphorylation. LC-SF-14 inhibits the proliferation of KATOIII cancer cells (IC50: 9.2 nM). LC-SF-14 has antitumor activity in the SNU-16 xenograft mouse model. LC-SF-14 can be used in FGFR2-driven gastric cancer research.

LC3B recruiter 2 (34R) is an LC3B recruiter and a component of the autophagy-lysosome pathway degradation system (ATTEC, Autophagy-Tethering Compounds), which directly binds to LC3B. LC3B recruiter 2 binds to CDK9 inhibitor SNS-032 through a linker, forming an ATTEC that targets the degradation of the CDK9 and Cyclin T1 complex (with inhibitory effects on both). Therefore, LC3B recruiter 2 exerts activity through the LC3B-dependent autophagy-lysosome pathway, interfering with the cell cycle of cancer cells, thus exhibiting antitumor activity.