Mal-C4-NH-Boc is a alkyl ether-based linker for PROTACs which joins two essential ligands, crucial for forming PROTAC molecules. This linker enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells.
Thalidomide-O-amido-C4-NH2 (Cereblon Ligand-Linker Conjugates 6) is a synthesized ligand-linker conjugate that combines a Thalidomide-based cereblon ligand with a linker. It functions as an E3 ligase ligand-linker conjugate and finds applications in the synthesis of PROTACs[1].
Lenalidomide-C4-NH2 hydrochloride is a Cereblon ligand derived from Lenalidomide. It serves as a recruiting agent for the CRBN protein. The compound, known as PROTAC (Compound 24), can be formed by linking Lenalidomide-C4-NH2 hydrochloride to the ligand for the protein. It exhibits inhibitory effects with IC50s of 0.98 nM and 13.7 nM against the growth of RS4;11 and MOLM-13 acute leukemia cell lines, respectively[1].
Pomalidomide-amido-C4-amido-PEG2-C2-NH-Boc is a novel synthesized conjugate compound functioning as an E3 ligase ligand-linker in PROTAC technology. This compound incorporates a Pomalidomide-derived cereblon ligand, which binds selectively to the E3 ligase cereblon, and a 2-unit PEG linker, which provides stability and flexibility to the conjugate.
Pomalidomide-amido-C4-amido-C6-NH-Boc, a synthesized conjugate, is a ligand-linker incorporating the cereblon ligand based on Pomalidomide and a PROTAC technology linker.
The chemical compound Mal-Phe-C4-Val-Cit-PAB-DMEA is a cleavable antibody-drug conjugate (ADC) linker that incorporates a Maleimide group. It is commonly employed in the synthesis of ADCs.
Mal-Phe-C4-Val-Cit-PAB is a cleavable antibody-drug conjugate (ADC) linker featuring a Maleimide functional group. It is employed in the synthesis of ADCs.
Mal-Phe-C4-VC-PAB-DMEA-PNU-159682 is a drug-linker conjugate utilized in antibody-drug conjugate (ADC) therapy. It comprises the ADC linker Mal-Phe-C4-VC-PAB and the potent ADC cytotoxin DMEA-PNU-159682. DMEA-PNU-159682 encompasses metabolites of nemorubicin (MMDX) derived from liver microsomes, as well as the ADC cytotoxin PNU-159682[1].
Mal-Phe-C4-VC-PAB-MMAE is a chemical compound resulting from the conjugation of monomethyl auristatin E (MMAE), a potent tubulin inhibitor serving as a toxin payload in antibody-drug conjugates, with a Mal-Phe-C4-VC-PAB linker.
(S,R,S)-AHPC-C4-NH2 dihydrochloride is a chemically derived E3 ligase ligand-linker conjugate, consisting of the (S,R,S)-AHPC VHL ligand and a linker specifically designed for EED-Targeted PROTAC[1].
(S,R,S)-AHPC-C4-NH2 is a custom-synthesized conjugate of an E3 ligase ligand-linker, which combines the VHL ligand based on (S,R,S)-AHPC and a linker specifically designed for EED-Targeted PROTAC[1].
Thalidomide-NH-C4-NH2 TFA (compound 29c) is a conjugate consisting of an E3 ligase ligand-linker, incorporating the Thalidomide-based cereblon ligand and a linker moiety. This compound, Thalidomide-NH-C4-NH2 TFA, is utilized as a component in PROTAC BRD2 BRD4 degrader-1, which is a highly potent and selective degrader targeting BET proteins BRD4 and BRD2[1].
Lipoxin C4 is a bioactive autacoid metabolites of arachidonic acid made by various cell types. It is categorized as a nonclassic eicosanoid and member of the specialized pro-resolving mediator (SPMs) family of polyunsaturated fatty acid (PUFA) metabolites
11-trans Leukotriene C4 (11-trans LTC4) is a C-11 double bond isomer of LTC4. LTC4 undergoes slow temperature-dependent isomerization to 11-trans LTC4 during storage. 11-trans LTC4 is produced in smaller amounts relative to LTC4 in ionophore-stimulated HMC-1 cells (a human mast cell line) and equine eosinophils, but not in human neutrophils or RBL-1 cells. It is nearly equipotent with LTC4 for contraction of guinea pig parenchymal and ileum. In a radioligand binding assay using guinea pig ileum as a cysteinyl leukotriene receptor preparation, the pKis for LTC4 and 11-trans LTC4 were determined to be 6.42 and 6.58, respectively.
C4 Ceramide is a bioactive sphingolipid and cell-permeable analog of naturally occurring ceramides. [1] [2] [3] It inhibits IL-4 production by 16% in EL4 T cells stimulated with phorbol 12-myristate 13-acetate when used at a concentration of 10 μM. [1] C4 Ceramide is cytotoxic to SK-BR-3 and MCF-7 Adr breast cancer cells (IC50s = 15.9 and 19.9 μM, respectively). [2] C4 Ceramide also increases maturation and stability of cystic fibrosis transmembrane conductance regulator (CFTR) proteins bearing the F508 deletion (F508del) mutation, enhances cAMP-activated chloride secretion, and suppresses secretion of IL-8 in primary epithelial cells isolated from patients with cystic fibrosis.[3]
Leukotriene C4 (LTC4) is the parent cysteinyl-leukotriene produced by the LTC4 synthase-catalyzed conjugation of glutathione to LTA4. LTC4 is produced by neutrophils, macrophages, and mast cells, and by transcellular metabolism in platelets. It is one of the constituents of slow-reacting substance of anaphylaxis (SRS-A) and exhibits potent smooth muscle contracting activity. LTC4-induced bronchoconstriction and enhanced vascular permeability contribute to the pathogenesis of asthma and acute allergic hypersensitivity. The concentration of LTC4 required to produce marked contractions of lung parenchymal strips and isolated tracheal rings is about 1 nM. LTC4 methyl ester is a more lipid soluble form of LTC4. The biological activity of LTC4 methyl ester has not been reported.
Produced by neutrophils, macrophages, mast cells, and by transcellular metabolism in platelets, leukotriene C4 (LTC4) is the parent cysteinyl leukotriene formed by the LTC4 synthase-catalyzed conjugation of glutathione to LTA4. It is one of the constituents of slow-reacting substance of anaphylaxis (SRS-A) and exhibits potent smooth muscle contracting activity. LTC4, however, is rapidly metabolized to LTD4 and LTE4, which makes the characterization of LTC4 pharmacology difficult. N-methyl Leukotriene C4 (N-methyl LTC4) is a synthetic analog of LTC4 that is not readily metabolized to LTD4 and LTE4.It acts as a potent and selective CysLT2 receptor agonist exhibiting EC50 values of 122 and > 2,000 nM at the human CysLT2 and CysLT1 receptors, respectively. It has essentially the same potency as LTC4 at both the human and murine receptors CysLT2 receptors. N-methyl LTC4 is potent and active in vivo, causing vascular leak in mice overexpressing the human CysLT2 receptor but not in CysLT2 receptor knockout mice.