ubiquitylation

By Targets:	Adrenergic Receptor (1) APC (1) Btk (1) Deubiquitinase (1) E1/E2/E3 Enzyme (5) EGFR (1) Estrogen Receptor/ERR (1) IKK (1) MDM-2/p53 (1) NF-κB (1) PINK1/Parkin (1) PROTACs (2) RIP kinase (2)
By Research Areas:	Cancer (10) Inflammation/Immunology (1)
Click Chemistry:	Azide (1)

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-123578

NSC689857	EGFR E1/E2/E3 Enzyme	Cancer
NSC689857 is a potent EGFR and SCF ^SKP2 inhibitor with an IC₅₀ value of 36 μM for Skp2-Cks1. NSC689857 can inhibit p27 ubiquitylation (IC₅₀=30 μM). NSC689857 has varied activity across cancer types, with more activity against leukemia cell lines than others .

HY-138642

Vepdegestrant 2 Publications Verification ARV-471	PROTACs Estrogen Receptor/ERR	Cancer
Vepdegestrant (ARV-471) is an orally active PROTAC estrogen receptor degrader against breast cancer. Vepdegestrant is a hetero-bifunctional molecule that facilitates the interactions between estrogen receptor alpha and an intracellular E3 ligase complex. Vepdegestrant leads to the ubiquitylation and subsequent degradation of estrogen receptors via the proteasome. Vepdegestrant robustly degrades ER in ER-positive breast cancer cell lines with a half-maximal degradation concentration (DC₅₀) of about 2 nM .

HY-110287

Apcin 3 Publications Verification	APC	Cancer
Apcin, a ligand of Cdc20, is a potent and competitive anaphase-promoting complex/cyclosome (APC/C(Cdc20)) E3 ligase activity inhibitor. Apcin competitively inhibits APC/C-dependent ubiquitylation by binding to Cdc20 and preventing substrate recognition. Apcin occupes the D-box-binding pocket on the side face of the WD40-domain and can prolong mitosis .

HY-153357

NRX-0492	Btk	Cancer
NRX-0492 is an orally active and potent degrader of BTK. NRX-0492 catalyzes ubiquitylation and proteasomal degradation of BTK with DC₅₀≤0.2 nM and DC₉₀≤0.5 nM, respectively. NRX-0492 inhibits B-cell receptor (BCR)-mediated signaling, transcriptional programs, and chemokine secretion. Moreover, NRX-0492 also links a noncovalent BTK-binding domain to Cereblon. Cereblon is an adaptor protein of the E3 ubiquitin ligase complex .

HY-18327

HLI98C

E1/E2/E3 Enzyme MDM-2/p53 Cancer

HLI98C is a ubiquitin ligase inhibitor. HLI98C inhibits p53 ubiquitylation. HLI98C inhibits HDM2 auto-ubiquitylation .
HY-19817

PRT4165

Maximum Cited Publications

6 Publications Verification

NSC600157
E1/E2/E3 Enzyme Cancer

PRT4165 is a potent inhibitor of PRC1-mediated H2A ubiquitylation.

HLI98C	E1/E2/E3 Enzyme MDM-2/p53	Cancer
HLI98C is a ubiquitin ligase inhibitor. HLI98C inhibits p53 ubiquitylation. HLI98C inhibits HDM2 auto-ubiquitylation .

PRT4165 Maximum Cited Publications 6 Publications Verification NSC600157	E1/E2/E3 Enzyme	Cancer
PRT4165 is a potent inhibitor of PRC1-mediated H2A ubiquitylation.

HY-145337

FT3967385 FT385	PINK1/Parkin Deubiquitinase	Cancer
FT3967385 is a novel USP30 inhibitor that recapitulates genetic loss of USP30 and sets the trigger for PINK1-PARKIN amplification of mitochondrial ubiquitylation.

HY-18937

WEHI-345 2 Publications Verification	RIP kinase	Cancer
WEHI-345 is a potent and selective RIPK2 kinase inhibitor with an IC₅₀ of 0.13 μM, which delays RIPK2 ubiquitylation and NF-κB activation on oligomerization domain (NOD) stimulation .

HY-100112

WEHI-345 analog	RIP kinase	Others
WEHI-345 analog is the analog of WEHI-345. WEHI-345 is a potent and selective RIPK2 kinase inhibitor with an IC₅₀ of 0.13 μM, which delays RIPK2 ubiquitylation and NF-κB activation on oligomerization domain (NOD) stimulation .

HY-110261

GS143	IKK E1/E2/E3 Enzyme NF-κB	Inflammation/Immunology
GS143 is a selective IκBα ubiquitination inhibitor with an IC₅₀ of 5.2 μM for SCF ^βTrCP1-mediated IκBα ubiquitylation. GS143 suppresses NF-κB activation and transcription of target genes and does not inhibit proteasome activity. GS143 has anti-asthma effect .

HY-126539

UBE2T/FANCL-IN-1	E1/E2/E3 Enzyme	Cancer
UBE2T/FANCL-IN-1 is a potent inhibitor of UBE2T/FANCL-mediated FANCD2 monoubiquitylation that sensitizes cells to the DNA cross-linking agent, Carboplatin .

HY-147100

α1A-AR Degrader 9c	PROTACs Adrenergic Receptor	Cancer
α1A-AR Degrader 9c (compound 9c) is a potent, selective and reversible α1A-AR (Adrenergic receptor) PROTAC degrader, with a DC₅₀ of 2.86 μM. α1A-AR Degrader 9c induces α1A-AR degradation can be attributed to proteasomal degradation. α1A-AR Degrader 9c inhibits the proliferation of PC-3 cells, with an IC₅₀ of 6.12 μM. α1A-AR Degrader 9c shows antitumor activity, and can be used for prostate cancer research .

Cat. No.	Product Name

HY-L024

Histone Modification Research Compound Library	612 compounds
A histone modification, a covalent post-translational modification (PTM) to histone proteins, includes methylation, phosphorylation, acetylation, ubiquitylation, and sumoylation, etc. In general, histone modifications are catalyzed by specific enzymes that act predominantly at the histone N-terminal tails involving amino acids such as lysine or arginine, as well as serine, threonine, tyrosine, etc. The PTMs made to histones can impact gene expression by altering chromatin structure or recruiting histone modifiers. Histone modifications act in diverse biological processes such as transcriptional activation/inactivation, chromosome packaging, and DNA damage/repair. Deregulation of histone modification contributes to many diseases, including cancer and autoimmune diseases. MCE owns a unique collection of 612 bioactive compounds targeting Epigenetic Reader Domain, HDAC, Histone Acetyltransferase, Histone Demethylase, Histone Methyltransferase, Sirtuin, etc. Histone Modification Research Compound Library is a useful tool for histone modification research and drug screening.

Histone Modification Research Compound Library

612 compounds

A histone modification, a covalent post-translational modification (PTM) to histone proteins, includes methylation, phosphorylation, acetylation, ubiquitylation, and sumoylation, etc. In general, histone modifications are catalyzed by specific enzymes that act predominantly at the histone N-terminal tails involving amino acids such as lysine or arginine, as well as serine, threonine, tyrosine, etc. The PTMs made to histones can impact gene expression by altering chromatin structure or recruiting histone modifiers. Histone modifications act in diverse biological processes such as transcriptional activation/inactivation, chromosome packaging, and DNA damage/repair. Deregulation of histone modification contributes to many diseases, including cancer and autoimmune diseases.

MCE owns a unique collection of 612 bioactive compounds targeting Epigenetic Reader Domain, HDAC, Histone Acetyltransferase, Histone Demethylase, Histone Methyltransferase, Sirtuin, etc. Histone Modification Research Compound Library is a useful tool for histone modification research and drug screening.

Cat. No.	Product Name		Classification

HY-148835

AzGGK		Azide
AzGGK is an unnatural amino acid. AzGGK is site-specifically incorporated into proteins via genetic-code expansion. AzGGK can be used as site-specific probe for ubiquitylation and SUMOylation . AzGGK is a click chemistry reagent, it contains an Azide group and can undergo copper-catalyzed azide-alkyne cycloaddition reaction (CuAAc) with molecules containing Alkyne groups. Strain-promoted alkyne-azide cycloaddition (SPAAC) can also occur with molecules containing DBCO or BCN groups.

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