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TC-E3 5032

* Please kindly note that our products are not to be used for therapeutic purposes and cannot be sold to patients.

TC-E3 5032 is a linker used in PROTAC technology that can be used in the synthesis of HDAC6 and anaplastic lymphoma kinase (ALK) degraders.

Category
Peptide Synthesis Reagents
Catalog number
BAT-006490
CAS number
835616-60-9
Molecular Formula
C13H9FN2O4
Molecular Weight
276.22
TC-E3 5032
Size Price Stock Quantity
5 g $439 In stock
IUPAC Name
2-(2,6-dioxopiperidin-3-yl)-4-fluoroisoindole-1,3-dione
Synonyms
E3 ligase Ligand 4; 1H-Isoindole-1,3(2H)-dione, 2-(2,6-dioxo-3-piperidinyl)-4-fluoro-; Thalidomide 4-fluoride; Thalidomide fluoride; 4-Fluoro-thalidomide; Cereblon ligand 4;E3 ligase Ligand 4; 2-(2,6-Dioxo-3-piperidinyl)-4-fluoro-1H-isoindole-1,3(2H)-dione
Appearance
White to Off-white Solid to Pale Purple Solid
Purity
≥ 98%
Density
1.570±0.06 g/cm3 (Predicted)
Melting Point
254-256 °C
Boiling Point
520.9±45.0 °C (Predicted)
Storage
-20 °C
Solubility
Slightly soluble in Dichloromethane (Heated), DMSO
InChI
InChI=1S/C13H9FN2O4/c14-7-3-1-2-6-10(7)13(20)16(12(6)19)8-4-5-9(17)15-11(8)18/h1-3,8H,4-5H2,(H,15,17,18)
InChI Key
CRAUTELYXAAAPW-UHFFFAOYSA-N
Canonical SMILES
C1CC(=O)NC(=O)C1N2C(=O)C3=C(C2=O)C(=CC=C3)F
1. Microenvironment in subchondral bone: predominant regulator for the treatment of osteoarthritis
Wenhui Hu, Shiwu Dong, Yueqi Chen, Ce Dou Ann Rheum Dis . 2021 Apr;80(4):413-422. doi: 10.1136/annrheumdis-2020-218089.
Osteoarthritis (OA) is a degenerative joint disease in the elderly. Although OA has been considered as primarily a disease of the articular cartilage, the participation of subchondral bone in the pathogenesis of OA has attracted increasing attention. This review summarises the microstructural and histopathological changes in subchondral bone during OA progression that are due, at the cellular level, to changes in the interactions among osteocytes, osteoblasts, osteoclasts (OCs), endothelial cells and sensory neurons. Therefore, we focus on how pathological cellular interactions in the subchondral bone microenvironment promote subchondral bone destruction at different stages of OA progression. In addition, the limited amount of research on the communication between OCs in subchondral bone and chondrocytes (CCs) in articular cartilage during OA progression is reviewed. We propose the concept of 'OC-CC crosstalk' and describe the various pathways by which the two cell types might interact. Based on the 'OC-CC crosstalk', we elaborate potential therapeutic strategies for the treatment of OA, including restoring abnormal subchondral bone remodelling and blocking the bridge-subchondral type H vessels. Finally, the review summarises the current understanding of how the subchondral bone microenvironment is related to OA pain and describes potential interventions to reduce OA pain by targeting the subchondral bone microenvironment.
2. Human NLRP1: From the shadows to center stage
Veit Hornung, Stefan Bauernfried J Exp Med . 2022 Jan 3;219(1):e20211405. doi: 10.1084/jem.20211405.
In response to infection or cell damage, inflammasomes form intracellular multimeric protein complexes that play an essential role in host defense. Activation results in the maturation and subsequent secretion of pro-inflammatory cytokines of the IL-1 family and a specific cell death coined pyroptosis. Human NLRP1 was the first inflammasome-forming sensor identified at the beginning of the millennium. However, its functional relevance and its mechanism of activation have remained obscure for many years. Recent discoveries in the NLRP1 field have propelled our understanding of the functional relevance and molecular mode of action of this unique inflammasome sensor, which we will discuss in this perspective.
3. Tuberculous bronchopleural fistula
Sarah C Boyd, Alexandra G A Stewart Respirol Case Rep . 2021 Mar 15;9(4):e00740. doi: 10.1002/rcr2.740.
Tuberculous bronchopleural fistula is a rare complication of pulmonary tuberculosis with presentation ranging from patients who are asymptomatic with incidental findings on imaging to those who present with acute tension pneumothorax.
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