CDK4 Inhibitor

CDK2/4 ligand 1 is a ligand for target protein for PROTACs, which targets CDK2/4. CDK2/4 ligand 1 can be used for synthesis of PROTAC CDK2/4 Degrader-1 (HY-179688).

CDK4/9-IN-1 (Compound 29) is a selective dual CDK4/9 inhibitor with IC₅₀ values of 23 nM and 12 nM, respectively. CDK4/9-IN-1 is promising for research of cancers.

CDK4/6-IN-23 (Compound 42) is a potent and selective CDK4/6 inhibitor, with an IC₅₀ of 11 nM for CDK6. CDK4/6-IN-23 can significantly activate immune cells and promote the production of IL-3. CDK4/6-IN-23 has dual myeloprotective and immunomodulatory effects in 5-FU (HY-90006) chemotherapy mice.

CDK4/6-IN-28 is a potent, orally active, and selective CDK4/6 inhibitor IC₅₀ values of 14.02 and 10.03 nM, respectively. CDK4/6-IN-28 inhibits breast cancer cell colony formation, migration, and proliferation. CDK4/6-IN-28 induces G1-phase cell cycle arrest and apoptosis in breast cancer cells. CDK4/6-IN-28 exhibits tumor inhibitory activity in breast cancer xenograft mouse models. CDK4/6-IN-28 can be used for the research of breast cancer.

CDK4/6-IN-7 is a potent, selective and orally active CDK4/6 inhibitor, with IC₅₀s of 1.58 and 4.09 nM, respectively. CDK4/6-IN-7 can be used for the research of breast cancer.

CDK4-IN-7 is a CDK4 inhibitor with an IC₅₀ of 26 nM. CDK4-IN-7 shows selectivity for CDK1, with an IC₅₀ of 4.2262 μM. CDK4-IN-7 can be used in cancer research.

Thio-acridone (SACD) is a photosensitizer (HAF-PSs). Thio-acridone forms a long-lived triplet state upon excitation by 470 nm visible light,, ultimately generating singlet oxygen to damage the structures and functions of target cells such as cancer cells. Thio-acridone is promising for research of cancers. Thio-acridone is a CDK4/Cyclin D1 inhibitor (IC50 = 2 uM).

PF-06842874 is a CDK4/Cyclin D1 and CDK6/Cyclin D3 inhibitor (K_i values are 62 and 130 nM, respectively). PF-06842874 can be used in the research of pulmonary arterial hypertension and cancer.

CDKI-83 is a potent CDK9 and CDK1 inhibitor with K_i values of 21 nM and 72 nM for CDK9/T1 and CDK1/B, respectively. CDKI-83 demonstrates effective anti-proliferative activity in human tumour cell lines with a GI₅₀<1 μM. CDKI-83 effectively induces apoptosis in A2780 human ovarian cancer cells. CDKI-83 reduces phosphorylation at Ser-2 of RNA polymerase II (RNAPII) by inhibiting cellular CDK9 activity, and down-regulates Mcl-1 and Bcl-2. CDKI-83 has the potential for anti-cancer research.

LCI133 is afirst-in-class,nanomolar-potent, selective multikinase inhibitor targeting CDK4/6/9 and AURKA/B (IC₅₀ = 4.7/10.2/4.1 nM and 2.8/10.6 nM). LCI133 induces S/G2 cell-cycle arrest and robust apoptosis in MYCN-amplified neuroblastoma BE(2)-C cells. LCI133 demonstrates significant antitumor efficacy in a BE(2)-C neuroblastoma xenograft model.

CDK4/6-IN-21 maleate (compound I-52) is a CDK4/6 inhibitor with IC₅₀ values of 3.88 and 3.31 nM for CDK4 and CDK6, respectively. CDK4/6-IN-21 maleate has antitumor activity.

CDK4/6-IN-20 (Compound II-5) is a CDK4/CDK6 inhibitor with IC₅₀ values ​​of 1.9, 14.2 nM, respectively. CDK4/6-IN-20 also inhibits cell proliferation and can be used in cancer research.

Palbociclib-C4-Boc is a Target Protein Ligand-Linker Conjugate that incorporates a ligand for CDK4/6 Palbociclib (HY-50767) and a PROTAC linker (HY-W007803), which recruits E3 ligases. Palbociclib-C4-Boc can be used for synthesis of PROTAC BSJ-03-204 (HY-136250).

G721-0282 is an orally active CHI3L1 inhibitor. G721-0282 can reduce the expression of inflammatory proteins and cytokines. G721-0282 inhibits the activation of the NF-κB signaling pathway. G721-0282 inhibits neuroinflammation and reduces anxious behavior. G721-0282 significantly inhibits the proliferation of osteosarcoma (OS) cells by suppressing the STAT3 signaling pathway. G721-0282 induces OS cell apoptosis by upregulating pro-apoptotic protein levels and downregulating anti-apoptotic protein levels. G721-0282 can be used for researches on neuroinflammatory conditions and cancer.

VWK147 is a second-generation HSP90 C-terminal domain (CTD) inhibitor. VWK147 targets the CTD dimerization interface, prevents HSP90 CTD dimerization, disrupts co-chaperone PPID binding to HSP90 CTD, and inhibits HSP90 chaperone function dependent on dimerization. VWK147 reduces protein levels of HSP90 client proteins ULK1, RIPK1, and CDK4 without inducing a heat shock response. VWK147 induces cell death, including apoptosis, in Cisplatin (HY-17394)-sensitive and -resistant urothelial carcinoma cells. VWK147 induces LC3-II accumulation, inhibits autophagosome-lysosome fusion to block canonical autophagy, and induces non-canonical LC3 lipidation independent of ULK1 and PIK3C3 complexes. VWK147 can be used for the research of urothelial carcinoma.

CDK2/4/6-IN-1(example 29) is a CDK2/4/6 inhibitor with IC₅₀ values of 2.5, 23.7 and 44.3 nM for CDK2, CDK4 and CDK6, respectively. CDK2/4/6-IN-1 can be used in cancer research. CDK2/4/6-IN-1 is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.

Radicicol 6-oxime (KF25706) is an Hsp90 inhibitor with an EC₅₀ of 5.5 nM against human Hsp90. Radicicol 6-oxime binds to Hsp90 and disrupts its chaperone function, leading to destabilization and depletion of Hsp90-associated signaling molecules. Radicicol 6-oxime depletes Hsp90-associated signaling proteins such as Raf-1, v-src, p185erbB2, Cdk4, and mutant p53, thereby inhibiting K-ras and v-src signaling pathways. Radicicol 6-oxime exhibits antiproliferative activity against various tumor cells. Radicicol 6-oxime inhibits tumor growth in mouse tumor xenograft models. Radicicol 6-oxime can be used for research on breast cancer, colon cancer, and vulvar epidermoid carcinoma.

PB1-3 is an orally active CDK4/CDK6 inhibitor with selective antiproliferative activity against 4T1 and MCF-7 breast cancer cells. PB1-3 directly binds to CDK4 and CDK6, downregulates total protein expression, reduces Rb phosphorylation, and induces G0/G1 phase arrest. PB1-3 induces ROS accumulation, mitochondrial membrane potential collapse, initiation of mitochondria-mediated intrinsic apoptosis, upregulation of the Bax/Bcl-2 ratio, and activation of cleaved caspase-3. PB1-3 inhibits tumor growth in a 4T1 orthotopic syngeneic mouse model. PB1-3 can be used for research related to triple-negative breast cancer.

CDK4/6-IN-29 is an orally active and highly selective CDK4/6 inhibitor, with an IC₅₀ of 3.17 nM against CDK4 and an IC₅₀ of 4.91 nM against CDK6. CDK4/6-IN-29 induces apoptosis in non-small cell lung cancer cells, inhibits cancer cell migration, induces G1-phase cell cycle arrest, and exhibits anti-tumor efficacy in vivo. CDK4/6-IN-29 can be used for research related to non-small cell lung cancer.

CDK4-IN-5 is a potent, orally active and selective CDK4 inhibitor. CDK4-IN-5 suppresses CDK4 expression and downregulates the CDK4/CyclinD1 complex. CDK4-IN-5 induces G₀/G₁ phase cell cycle arrest in bladder cancer cells via CyclinD1 expression suppression. CDK4-IN-5 selectively exerts activity against bladder cancer cells. CDK4-IN-5 can be used for the research of bladder cancer.