ARCC-4

Protein target name:

Mechanism of action:

DegraderPROTAC

Recommended Concentration for use in cells:

> 50 nM

Probe Availability

MedChemExpress

Probe Information

Target and Probe Information

Target Details

Target class:

Transcription factor

Subclass:

Nuclear Hormone Receptor

HUGO ID:

HGNC:644

Entrez gene ID:

367

UNIPROT ID:

P10275

Target alias:

KD; AIS; AR8; TFM; DHTR; SBMA; HYSP1; NR3C4; SMAX1; HUMARA

Probe Details

Chemical Probes Portal ID:

CPP2134

Probe alias:

PROTAC, cpd 2c

PubChem CID:

122428515

ChEMBL ID:

CHEMBL4540528

SMILES string:

O=C(NCC1=CC=C(C2=C(C)N=CS2)C=C1)[C@H]3N(C([C@H](C(C)(C)C)NC(COCCCCOC4=CC=C(C5=CC=C(N(C(N6C7=CC=C(C#N)C(C(F)(F)F)=C7)=S)C(C)(C)C6=O)C=C5)C=C4)=O)=O)C[C@H](O)C3

InChi Key:

DUPAJELXESPTNF-PPZGWQTASA-N

Control compound:

cpd 3

Orthogonal probe:

ARD-266

Validation in Cells and Model Organisms

In cell validation

On target activity in cells

Potency in cells:

DC50DmaxIC50

5 (DC50), 98%, 36 nM (IC50),

Potency assay (cells):

Western Blot, RL binding Assay (lysate), Cell Proliferation Assay

Phenotypic Control Experiment:

Degradation is proteasome dependent: AR degradation was blocked by epoxomicin, but was unaffected by bafilomycin, suggesting that ARCC-4 induces the degradation of AR in cells via the proteasome.

Off target activity in cells

Probe Selectivity in Cell:

@ 1 uM ARCC-4 had no effect on glucocorticoid receptor and estrogen receptor levels, while there was a modest decrease in progesterone receptor (PR) A and B levels in T47D cells.

Primary Reference

Reference (doi):

10.1038/s42003-018-0105-8

Reference (PMID):

30271980

ARCC-4

Probe Availability

Probe Information

Target Details

KD; AIS; AR8; TFM; DHTR; SBMA; HYSP1; NR3C4; SMAX1; HUMARA

Probe Details

In cell validation

Primary Reference

Supporting Organizations

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ARCC-4

Probe Availability

Probe Information

Target Details

KD; AIS; AR8; TFM; DHTR; SBMA; HYSP1; NR3C4; SMAX1; HUMARA

Probe Details

In cell validation

Primary Reference

Supporting Organizations

Interested in supporting the portal?