Cdk4 pAb
- Known as:
- Cdk4 pAb
- Catalog number:
- ASAKAS-CC008E
- Product Quantity:
- 100 µL
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- Cdk4 pAb
Ask about this productRelated genes to: Cdk4 pAb
- Gene:
- CDK4 NIH gene
- Name:
- cyclin dependent kinase 4
- Previous symbol:
- -
- Synonyms:
- PSK-J3
- Chromosome:
- 12q14.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-07-28
- Date modifiied:
- 2019-04-23
Related products to: Cdk4 pAb
Related articles to: Cdk4 pAb
- Lung cancer remains the leading cause of cancer-related mortality worldwide, responsible for over 1.8 million deaths annually. Despite therapeutic advancements, clinical outcomes in advanced lung adenocarcinoma (LUAD) remain poor due to treatment resistance and metastasis. Cyclin-dependent kinases (CDKs) are essential regulators of cell cycle progression and transcription, yet their therapeutic targeting-especially beyond CDK4 and CDK6-has been largely underexplored in lung cancer. This study investigates the oncogenic relevance of CDK1, CDK2, CDK5, CDK7, and CDK9 in LUAD and evaluates the effects of two pharmacological CDK inhibitors: Roscovitine (a broad-spectrum CDK inhibitor) and RO-3306 (a CDK1-selective inhibitor). - Source: PubMed
Publication date: 2026/06/16
Alsayyid AzizehGhemrawi RoseSammani NourRamadan AzzaKremesh SedraSakkal MolhamAldamook NosaybaMousa Walaa KKhair Mostafa - The cyclin-dependent kinase 6 (CDK6) is a central regulator of cell cycle progression and an important contributor to the development of acute leukemia, particularly in poor prognosis subtypes. Preclinical studies have demonstrated activity of CDK6-targeting drugs in acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL), but clinical trials with CDK4/6 inhibitors as monotherapy were disappointing. In contrast, clinical efficacy was observed for the combination of the dual CDK4/6 inhibitor, palbociclib, with chemotherapy in pediatric acute leukemia and lymphoma patients. We sought to evaluate the potential of CDK6 inhibition to sensitize AML cells to both standard-of-care and novel targeted therapies. We found the CDK2- targeting drug, tegtociclib, to be particularly effective in potentiating the inhibitory effects of CDK4/6 inhibitors against acute leukemia cells. While similar strategies have been considered for solid tumors where CDK4/6 targeted agents may work as monotherapy, we have discovered a unique and novel approach to introduce this class of drugs to acute leukemias. Our results also demonstrate that synergy between these agents, as has been previously shown in breast cancer, is also observed in acute leukemia and correlates with suppression of the Rb/E2F axis and inhibition of cell cycle progression. The universality between the underlying mechanisms of synergy for CDK2 inhibitors combined with CDK4/6 inhibitors in breast cancer and AML warrants further evaluation in other malignancies characterized by dependencies on these CDK subtypes. - Source: PubMed
Publication date: 2026/06/18
Weisberg EllenChowdhury BasudevGarg SwatiAkatsu TaiseiNi WeiGokhale Prafulla CEschle Benjamin KGrant SydneySattler MartinDeCaprio James ANöltner LukasGarcia JacquelineMarinchev KateGalinsky IleneNath AritroStone Richard MGriffin James D - This review explores strategies to overcome the clinical limitations of Cyclin-dependent kinases 4 and 6 (CDK4/6) inhibitors, namely, reversible cytostasis and acquired resistance. We outline an emerging therapeutic framework in which these inhibitors induce specific vulnerabilities, shifting the treatment objective from growth suppression toward tumor clearance. Specifically, we analyze the effects of CDK4/6 inhibitors across four interconnected domains: cellular senescence, compromised DNA damage repair, metabolic reprogramming, and immune microenvironment remodeling. Building upon this framework, we summarize rational combination strategiessuch as pairing with senolytics, poly-(ADP-ribose) polymerase (PARP) inhibitors, or immune checkpoint inhibitors (ICIs)designed to exploit these induced vulnerabilities. To bridge preclinical rationale with clinical application, we discuss key translational determinants, noting that successful implementation depends on biomarker-guided patient selection and optimized dosing schedules (e.g., sequential administration) to mitigate overlapping toxicities. Collectively, the evidence suggests that rational combination strategies could repurpose CDK4/6 inhibitor therapy for more durable tumor control. - Source: PubMed
Publication date: 2026/05/13
Ma CongJi XuanHuang WenqinGuo SenyangWang LingziWu XinhongZheng HongmeiWang Jingru - The treatment with cyclin-dependent kinase 4/6 inhibitors (CDK4/6i) (ribociclib, palbociclib, and abemaciclib) combined with endocrine therapy (ET) has become the standard of care (SoC) for first-line treatment in patients with metastatic hormone receptor-positive (HR+) and human epidermal growth factor receptor 2-negative (HER2-) breast cancer. There is a lack of consensus on what treatment to offer after disease progression, and there are no established guidelines for therapeutic sequencing. - Source: PubMed
Publication date: 2026/05/17
Freitas RitaBarroso TiagoBraga SofiaSantos Catarina CBatista MartaChaves AndreiaCabral SaraFortuna AnaPatel VanessaAraújo JoãoDuarte TâniaCabral Tiago PSilva SandraViana CláudiaBaptista CarlotaGonçalves JoanaDunões Inês QEiriz Inês - CDK4-selective inhibitors are emerging as promising anticancer agents. Relative to dual CDK4/6 inhibitors, CDK4-selective inhibitors have the potential to retain efficacy while improving tolerability. However, the therapeutic value and mechanistic consequences of selectively targeting CDK4 in prostate cancer remain largely undefined. Here, we investigated the anti-tumour activity and mode of action of the CDK4 inhibitors AU2-94 and atirmociclib across diverse prostate cancer models. - Source: PubMed
Publication date: 2026/06/17
Safaroghli-Azar AvaCroft TravisMekonnen Laychiluh BLenjisa JimmaDickel MajaShrestha Raj KSita SamyuktaChoo NicholasRoach MichaelBasnet Sunita K CLawrence Mitchell GSelth Luke AWang Shudong