Ginsenoside C-K (Ginsenoside K) is a bacterial metabolite of G-Rb1 exhibiting anti-inflammatory effects by reducing iNOS and COX-2.

Gracillin can induce cell cycle arrest, oxidative stress, and apoptosis in HL60 cells, and has the potential to be developed as an antitumor agent. Gracillin can be selected as lead compounds for the development of new drugs against I. multifiliis.

Schinifoline is a quinolone derivative extracted from Zanthoxylum schinifolium Sieb with cytotoxic activity that promotes radiosensitization of cancer cells, affects the cell cycle and apoptosis.

4-Oxofenretinide (3-Keto fenretinide) , a recently identified fenretinide metabolite, induces marked G2-M cell cycle arrest and apoptosis.

Kaempferitrin (Lespenephryl) has antidepressant-like effect related to the serotonergic system, principally 5-HT1A. Kaempferitrin exerts cytotoxic and antitumor effects against HeLa cells. Kaempferitrin stimulates glucose-metabolizing enzymes, promotes glucose homeostasis. Kaempferitrin exerts immunostimulatory effects on immune responses mediated by splenocytes, macrophages, PBMC and NK cells. Kaempferitrin induces cytotoxic effects to include: cell cycle arrest in G1 phase and apoptosis via the intrinsic pathway in a caspase-dependent pathway.

CAM 833 is an effective orthosteric inhibitor of the BRCA2-RAD51 interaction, inhibiting RAD51 aggregation, enhancing DNA damage-induced apoptosis, increasing 4N cell cycle arrest, and disrupting homologous DNA repair (HDR), and can be used for cancer therapy.

Trilaciclib is a short-acting, orally effective CDK4/6 inhibitor with IC₅₀ values of 1 nM and 4 nM respectively. It transiently and reversibly induces G1 cell cycle arrest, mitigates chemotherapy-induced myelosuppression, and enhances antitumour immunity, making it applicable across multiple cancers.

Picrasidine Q is an anticancer natural alkaloid that targets FGFR2, inducing apoptosis and G1 arrest in oesophageal squamous cell carcinoma (ESCC) cells.

Imofinostat (MPT0E028) is a selective, orally available pan-HDAC inhibitor with IC₅₀ values of 53.0/106.2/29.5 nM against HDAC1/HDAC2/HDAC6 in HCT116 cells. In B-cell lymphoma, Imofinostat induces cell cycle arrest and apoptosis whilst inhibiting Akt phosphorylation, demonstrating anticancer activity across multiple tumour types.

TH9619 is an effective inhibitor of both dehydrogenase and cyclohydrolase activities in MTHFD1 and MTHFD2 (IC50=47 nM). It induces folate trapping and cell cycle arrest, thereby selectively killing cancer cells expressing MTHFD2.

Anti-melanoma agent 1 (Compound 5m) is a 1-arylamino-3-aryloxypropan-2-ol derivative. It acts by disrupting microtubules, arresting cell cycle at G2/M phase, and inducing apoptosis in melanoma lines (IC50 = 1.98 - 3.70 μM).

GSK3735967 is a potent PRMT5 inhibitor. It blocks symmetric arginine dimethylation to interfere with oncogenic signaling and induce cell cycle arrest, used for hematological and solid tumor research.

Glychionide A is a flavonoid glycoside discovered in Glycyrrhiza glabra that exhibits antitumor activity against PANC-1 cells by inducing autophagy, apoptosis, cell cycle arrest, and disruption of mitochondrial membrane potential.

Ribociclib hydrochloride (LEE011 HCl) is a selective, orally active cyclin-dependent kinase CDK4/6 inhibitor (IC50=10/39 nM) that blocks cell cycle progression and inhibits tumor cell proliferation.

PRLX-93936 is a selective Ras pathway protein inhibitor that modulates RAS/JNK pathway-associated protein phosphorylation, induces caspase-dependent apoptosis and cell cycle arrest, and exhibits anticancer activity.

PEP1 acetate is a p21-mimetic peptide that serves as a specific proliferating cell nuclear antigen (PCNA) binding inhibitor. It arrests the cell cycle in the S phase by competitively blocking the interaction between PCNA and DNA polymerase delta, thereby interfering with DNA replication.

2-O-β-D-Glucopyranosyl-L-ascorbic acid (AA-2βG) is a natural and stable vitamin C analog that induces apoptosis and cell cycle arrest in cancer cells by stabilizing p53 protein.

PI-103 Hydrochloride is a dual PI3K/Akt and mTOR inhibitor exhibiting nM-level inhibition of p110α, p110β, p110δ, p110γ, DNA-PK, mTORC1, and mTORC2. PI-103 induces autophagy, mitochondrial apoptosis, and cell cycle arrest, making it suitable for leukaemia research.

S)-(-)-Perillic acid is a terpenoid natural product capable of inhibiting protein pentosylisation and protein acylation. It exhibits anti-infective and anti-cancer activity, inducing cell cycle arrest and apoptosis in non-small cell lung cancer cells while increasing intracellular protein levels of Bax, p21, and caspase-3.

INNO-220 is a molecular glue degrader targeting CK1α, exhibiting oral activity and CRBN dependency, capable of inducing cell cycle arrest at G0/G1 phase and apoptosis. INNO-220 disrupts the assembly and function of the CARD11/BCL10/MALT1 complex, inhibits the NF-κB signaling pathway, and activates the p53 pathway, making it suitable for lymphoma research.

Tubulin inhibitor 49 (Compound 18) is a tubulin polymerization inhibitor (IC50 = 48 μM) that disrupts the cellular microtubule network, arresting the cell cycle at G2 phase. It exhibits toxicity toward HeLa cells (IC50 = 8.8 μM).

MYF-03-69 (TEAD-IN-3) is a covalent and irreversible pan-TEAD inhibitor with IC₅₀ values of 385/143/558/173 nM for TEAD1/TEAD2/TEAD3/TEAD4, respectively. MYF-03-69 inhibits TEAD transcriptional activity (IC₅₀ = 56 nM), upregulates the pro-apoptotic gene BMF, and suppresses mesothelioma cancer cells with defective Hippo signaling, making it suitable for malignant pleural mesothelioma (MPM).

AC-4-130 is a direct STAT5 SH2 domain inhibitor that can disrupt STAT5 activation, dimerization, nuclear translocation, and STAT5-dependent gene transcription, inducing cell cycle arrest and apoptosis in leukemia cells, and can be used for the study of acute myeloid leukemia (AML).

Sodium citrate monobasic (Citric acid monosodium salt) is a biochemical reagent serving as a preservative, emulsifier, chelating agent, and buffer. Monobasic sodium citrate induces apoptosis in HaCaT cells and causes cell cycle arrest at the G2/M and S phases. It also induces hepatic oxidative damage by reducing antioxidant enzyme activity.