RP-1664 free base · Synonyms: RP 1664 · RP1664

RP-1664 is a selective and orally active PLK4 inhibitor.

For research use only. Not for human or veterinary use.

Target Polo-like Kinase (PLK)

Research area Cancer

Purity >98% Stock Inquire

Data Sheet SDS COA

RP-1664 structure

CAS No.: 2980682-00-4

Download structure (.mol)

Pack sizes & pricing

Size	Price	SKU	Stock
5 mg	USD 560.00	BP-02172-5mg	In stock	Get quote
10 mg	USD 880.00	BP-02172-10mg	In stock	Get quote
25 mg	USD 1,750.00	BP-02172-25mg	In stock	Get quote
50 mg	USD 2,750.00	BP-02172-50mg	In stock	Get quote

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Description

RP-1664 is a selective and orally active PLK4 inhibitor. RP-1664 drives potent synthetic lethality in TRIM37-high tumor models in vitro and in vivo. RP-1664 induces both centriole loss and amplification contribute to hypersensitivity of neuroblastoma cells.

Biological activity

In Vitro RP-1664 (1-1000 nM, 48-72 h) increases total PLK4 protein levels in RPE1-hTERT Cas9 TP53-null cells and increases p21 protein levels in RPE1-hTERT Cas9 TP53-WT cells dose dependently. RP-1664 (0.001-10 μM) demonstrates a ~30-fold increase in sensitivity between TRIM37-normal/TP53-KO cells and TRIM37-overexpressing/TP53-WT cells, with intermediate sensitivity observed in TRIM37-high/TP53-KO and TRIM37-normal/TP53-WT cells. RP-1664 (50-250 nM) induces centrosome loss at concentrations >100 nM in both p53-proficient and -deficient RPE1 cells as well as in three different NBL cell lines (CHP134, CHP212, SHSY5Y). RP-1664 (50-250 nM) induces supernumerary centrosomes between 25-100 nM in both p53-proficient and -deficient RPE1 cells[1]. RP-1664 (0-2000 nM, 48 h) enhances cellular sensitivity to PLK4 inhibition and centrosome depletion in a manner dependent on high TRIM37 protein levels and functional p53. RP-1664 (compound 37) shows an EC50 of 0.051 μM in reducing MCF7 cell viability. In Vivo RP-1664 (600 ppm, oral administration via feed, 7 days on/7 off or 14 days on/7 off or daily for 40 days) exhibits dose-dependent anti-tumor activity in MCF7 xenograft mice. RP-1664 (300 ppm, oral administration via feed, 17 days on/7 off for 40 days) elicits robust anti-tumor activity in NBL models through low-dose-induced centrosome amplification. RP-1664 (compound 37) (6-21 mg/kg, i.g., twice a day, 35 days) shows dose responsive tumor growth inhibition, stasis and regressions in CAL-148 xenograft mice. RP-1664 (300-600 ppm, oral administration via feed, 3 days on/4 off or 14 days on/7 off or daily for 55 days) inhibits tumor growth in CHP-134 xenograft mice.

Identifiers

SMILES: CC1=CC(NC2=NC(N(C3=C(C=C(C=C3F)S(C)(=O)=O)F)C)=NC(C4=CN(C=N4)C)=C2C5CC5)=NN1
InChIKey: POKVQQVLRJLUAK-UHFFFAOYSA-N

Specifications

MW (average): 514.5510
Formula: C₂₃H₂₄F₂N₈O₂S
CAS No.: 2980682-00-4
Physical state: Solid
Color: White to off-white
Shipping: Shipped under ambient temperature as non-hazardous chemical. This product is stable enough for a few weeks during ordinary shipping and time spent in Customs.
Storage: Pure form 4℃ 2 years; In solvent -20℃ 1 month;

Solubility

Soluble in DMSO

Documents

References

[1]. Isabel Soria-Bretones, et al. A dual mechanism of sensitivity to PLK4 inhibition by RP-1664 in neuroblastoma. bioRxiv. February 17, 2025.

[2]. Vallée F, et al. Discovery of RP-1664: A First-in-Class Orally Bioavailable, Selective PLK4 Inhibitor. J Med Chem. 2025 Jun 12;68(11):10631-10647.

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