Table 2.

Therapeutic targeting of condensates in cancer

Strategy	Reagent	Target	Effects	Refs
Targeting IDRs	Tin‐based metal cluster	TAF2 subunit of TFIID	Inhibit transcription initiation	[252]
	IIA4B20, IIA6B17, mycmycin‐1/2	c‐MYC	Inhibit MYC‐induced cell malignant transformation	[253, 254]
	YK‐4‐279	EWS‐FLI1 fusion	Block the interaction of EWS‐FLI1 and RNA helicase A and reduce EWS cells growth	[255]
	PRIMA‐1, APR‐246, ReACp53, Polyarginine	p53 mutants	Halt p53 mutants amyloid formation	[256, 257, 258]
	Elvitegravir	SRC1	Inhibit YAP oncogenic transcription	[259]
Decondensation or recondensation	1, 6‐hexanediol (HDO)	General solvent	Dissolve condensates directly	[79, 260]
	Lipoamide, Lipoic acid	General solvent	Dissolve FUS‐related SGs	[264]
	Bis‐ANS	Modulators of TDP‐43 condensates	Biphasic activity depends on the concentration	[265]
	C108	G3BP2	Reverse SGs‐mediated initiation of breast cancer	[262]
	Vinblastine	Microtubule	Dissolve SGs	[263]
	All‐trans retinoic acid, Arsenic trioxide	PML‐RARA fusion	Recover PML bodies in acute promyelocytic leukemia	[266]
	RNA silencing technology	RNAs	RNA‐driven formation of aberrant biomolecular condensates	[267]
Drug partition	Tamoxifen, Cisplatin, THZ1, JQ1	SEs	Actively partition into SEs and enhance the therapeutic activity	[261]
Disrupting the modifications	Olaparib	PARP1/2	Impairs PARylation‐related DNA repair condensates	[159]
	GSK‐626616	DYRK3	Inhibit PRAS40 phosphorylation and restrain mTORC1 signaling in SGs	[135, 269]
	SI‐2	NSD2	Abolish SRC3 methylation and sensitize bortezomib treatment	[271]
	JQ1	BRD4	Release the Mediator complex from SEs	[272]
	SGC0946	DOT1L	Inhibit histone H3K79 methylation and histone H4 acetylation	[273]
	THZ1	CDK7	Inhibit RNAPII phosphorylation	[17, 274]
	THZ531	CDK12 and CDK13	Inhibit RNAPII phosphorylation	[275]