IKZF1 antibody - middle region (ARP31470_P050)
- Known as:
- IKZF1 (anti-) - middle region (ARP31470_P050)
- Catalog number:
- arp31470_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- IKZF1 antibody - middle region (ARP31470_P050)
Related genes to: IKZF1 antibody - middle region (ARP31470_P050)
- Gene:
- IKZF1 NIH gene
- Name:
- IKAROS family zinc finger 1
- Previous symbol:
- ZNFN1A1
- Synonyms:
- hIk-1, LyF-1, Hs.54452, IKAROS, PPP1R92
- Chromosome:
- 7p12.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-08-23
- Date modifiied:
- 2019-04-23
Related products to: IKZF1 antibody - middle region (ARP31470_P050)
Related articles to: IKZF1 antibody - middle region (ARP31470_P050)
- Drugs targeting Bruton's tyrosine kinase (BTK) are recognized as key tools in hematological oncology. The clinical efficacy of BTK inhibitors is limited, however, by the emerging resistance driven by BTK mutations and the severe toxicity attributed to off-target kinase inhibition. PROteolysis TArgeting Chimeras (PROTACs) offer an alternative modality to address these major drawbacks. Herein, we present novel BTK-targeting PROTACs with a high potency against both the wild-type and the mutated BTK. Novel CRBN-binding warheads have been developed to mitigate the off-target protein degradation associated with anchors derived from thalidomide analogues. The linker optimization effort resulted in a series of potent, orally bioavailable BTK-targeting PROTACs without concomitant activity against IKZF1, IKZF3, and GSPT1. The lead compounds ISM-PR25 and ISM-PR44 demonstrate sufficient efficacy in degrading BTK protein in malignant B cells (DC50 = 0.04 and 0.05 nM, respectively) associated with a favorable DMPK profile and a large safety window regarding cell toxicity and effectively degraded BTK in mouse circulating B cells by single-dose oral treatment (3 mg/kg). - Source: PubMed
Mantsyzov Alexey BZhao PeiKruse Chris GPetrov RostislavHuang FubaoYu JiaojiaoCai XinDing XiaoAladinskiy VladimirAliper AlexRen FengZhavoronkov Alex - Bromodomain-containing protein 9 (BRD9) has emerged as an epigenetic target in hematologic malignancies. However, previous studies on BRD9 PROTACs reported MYC upregulation following chronic administration. Here, we describe bifunctional BRD9 PROTAC/immunomodulatory drug (IMiD) degraders engineered to simultaneously eliminate BRD9 and IKZF1. Utilizing ternary complex modeling and structure-activity relationship (SAR) analysis, aromatic linkers and modified E3 ligands facilitated efficient degradation. The lead candidate, B8, induces potent and selective degradation of both BRD9 (DC50 = 57 pM) and IKZF1 (DC50 = 62 pM). B8 showed broad antiproliferative activity across hematologic malignancy cells, particularly lymphomas. In the OCI-ly10 xenograft model, B8 achieved near-complete tumor regression (TGI > 99%), significantly outperforming the selective BRD9 PROTAC E5 (TGI = 31%), without detectable toxicity or MYC upregulation. These findings validate this dual-targeting PROTAC/IMiD strategy as an effective approach to overcoming the limitations of selective BRD9 degraders, underscoring its therapeutic potential in hematologic malignancies. - Source: PubMed
Duan HaitingChen RuoxinZhang JingyuZhou HuanLi BizhiZhai XiangyingWang HanlinJiang RongkuanSong JiangzhouLi JiaChe JinxinZhou YuboDong Xiaowu - Common variable immunodeficiency (CVID) is the most common clinically significant primary antibody deficiency in adults, characterized by impaired immunoglobulin production and recurrent infections. Endocrinopathies represent a substantial burden in inborn errors of immunity, with reported prevalence rates of approximately 27-32.5%. Existing literature on CVID has focused mainly on autoimmune endocrinopathies, and no study has specifically evaluated endocrine disorders in adult CVID patients. This gap is clinically important because these patients may have non-autoimmune endocrinopathies as well as glucocorticoid -induced endocrinopathies due to long-term steroid therapy. We aimed to evaluate endocrinopathies in adult CVID patients and identify associated factors and genetic characteristics. - Source: PubMed
Publication date: 2026/08/24
Yigitdol IsmailColkesen FatihGerek Mehmet EminYilmaz Ergun UmmugulsumKolak SecimHarman EmrahSagun FerhatAslan Savas SukranArslan Sevket - WHO5 (2022) classification of B-lymphoblastic leukemia (B-ALL) incorporates several novel entities requiring high-throughput sequencing for their accurate characterization. The clinical relevance of this classification in the context of contemporary measurable residual disease (MRD)-directed therapy is unclear. - Source: PubMed
Publication date: 2026/09/03
Rajpal SwetaChatterjee GauravBhanshe PrasannaTerse VishramJoshi SwapnaliChaudhary ShrutiShetty DhanalaxmiMohanty PurviDhamne ChetanTembhare Prashant RameshSrinivasan ShyamChichra AkankshaMoulik Nirmalya RoyBanavali ShripadGujral SumeetNarula GauravSubramanian Papagudi GPatkar Nikhil - Regulation of oncogenic transcriptional programs in multiple myeloma requires the interplay of histone modifications, their writers and readers with lineage-affiliated transcription factors. The transcription factors IKZF1/3, IRF4 and MYC form an aberrant, myeloma-specific regulatory loop that drives myelomagenesis and resistance to immunomodulatory drugs (IMiDs) such as lenalidomide. Chromatin-based mechanisms that regulate these processes remain incompletely understood. Here we investigate the role of CXXC1, a core component of the H3K4 methyltransferase complex COMPASS, in the activity of the IKZF1/3-IRF4-MYC regulatory loop. We find that clinically, high CXXC1 expression is associated with high-risk proliferative, adverse prognosis disease. Consistent with this, CXXC1 is a myeloma dependency and it regulates cellular fitness programs including cell cycle, MYC targets and DNA damage response. High CXXC1 expression in primary myeloma cells is associated with higher chromatin accessibility, while acute depletion of degron-tagged CXXC1 further validates its role in regulating myeloma cell fitness programs and high-risk transcriptional signatures. CXXC1 interacts with and extensively co-binds to chromatin with IRF4 and IKZF3. Notably, in both lenalidomide-sensitive and -resistant myeloma cells, CXXC1 depletion results in loss of IRF4 and IKZF3 chromatin binding and in parallel it 'breaks' the IRF4 transcriptional self-regulatory loop. Thus, CXXC1 and COMPASS emerge as novel therapeutic targets in IMiD-sensitive and -resistant myeloma by regulating the activity of IRF4 and essential myeloma cell fitness programs. - Source: PubMed
Publication date: 2026/09/02
Sabbattini Pierangela M RTrasanidis NikolaosTaslim JasonWhitwell HarryHuang YimingCaputo Valentina SNg Han LengChaidos AristeidisFordwor-Hepburn KatrinaJia QizhenKatsarou AlexiaAtta MariaBua MarcoRos-Soto JoseRoberts IreneFeldhahn NiklasCrump NicholasKaradimitris Anastasios