DS17 |CAS|DC Chemicals

Cas No.:
Chemical Name:	DS17
SMILES:	CC(C)N(C=N1)C2=C1C(NCC3=NC(C=C(Cl)C(Cl)=C4)=C4N3)=NC(N[C@H](CC)CO)=N2
Formula:	C₂₀H₂₄Cl₂N₈O
M.Wt:	463.36
Purity:	>98%
Sotrage:	2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO

MSDS

Cat. No.	Product name	Field of application
DC67413	MRT-23227
DC67412	MRT-3486
DC67411	MRT-7612
DC67410	MRT-10350
DC67407	IKZF1-degrader-1	IKZF1-degrader-1 (Compound 9-B) is a highly potent molecular glue that achieves sub-nanomolar degradation of IKZF1 (DC50 = 0.134 nM), demonstrating significant therapeutic potential for targeting IKZF1-dependent malignancies.
DC67406	EM12-FS	EM12-FS is a bifunctional CRBN modulator that engages cereblon at His353 while functioning as a molecular glue to induce NTAQ1 degradation. Demonstrating favorable pharmacokinetics, it exhibits a human plasma half-life of 196 minutes, supporting its therapeutic potential.
DC67405	Acetyl-cyclosporin A aldehyde	Acetyl-cyclosporin A aldehyde is a chemically modified derivative of cyclosporin A (HY-B0579), featuring an acetyl group and a reactive aldehyde moiety. The parent compound, cyclosporin A, is a dual-function molecule that both inhibits calmodulin signaling and binds cyclophilin, thereby blocking NF-AT nuclear translocation and inducing mitochondrial dysfunction.
DC67404	QS-57	QS-57 is a bifunctional degrader that combines BRD4-targeting PROTAC activity with 14-3-3 molecular glue properties.
DC67403	KRAS ligand 4	KRAS ligand 4 (compound 2) is a SOS1-targeting bifunctional molecular glue that suppresses oncogenic signaling by degrading key KRAS pathway components, evidenced by reduced pERK and pS6 levels. It demonstrates broad-spectrum activity against diverse KRAS mutations, disrupting proliferation across resistant cancer models.
DC67402	Pomalidomide-15N,13C5	Pomalidomide-15N,13C5 is a stable isotope-labeled variant of pomalidomide (HY-10984), a third-generation immunomodulatory drug that functions as a cereblon-directed molecular glue. This compound mediates targeted ubiquitination and degradation of Ikaros family transcription factors (IKZF1/3) through recruitment of the CRL4CRBN E3 ligase complex, underpinning its therapeutic mechanism.