IDH2 Antibodies

Isocitrate dehydrogenase [NADP], mitochondrial (IDH2)

Plays a role in intermediary metabolism and energy production. It might closely associate or interact with the pyruvate dehydrogenase complex.

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Gene Information

Human
Gene Name:	IDH2
Uniprot:	P48735
Entrez:	3418

Family

Belongs to:
isocitrate and isopropylmalate dehydrogenases family

Alternative Names

D2HGA2; EC 1.1.1.42; ICD-M; IDH; IDHM; IDP; IDPM; isocitrate dehydrogenase [NADP], mitochondrial; isocitrate dehydrogenase 2 (NADP+), mitochondrial; mNADP-IDH; NADP(+)-specific ICDH; Oxalosuccinate decarboxylase

Molecular Weight

Mass (kDA):
50.909 kDA

Genomic Context

Human
Location:	15q26.1
Sequence:	15; NC_000015.10 (90083045..90102468, complement)

Subcellular Localizations

Mitochondrion.

Diseases

• Neoplasms
• Glioma
• Leukemia
• Myeloid Leukemia
• Brain Neoplasms
• Leukemia, Myelocytic, Acute
• Malignant Neoplasms
• Glioblastoma
• Astrocytoma
• Oligodendroglioma
• Cell Transformation, Neoplastic
• Dysmyelopoietic Syndromes
• Malignant Paraganglionic Neoplasm

• Myeloproliferative Disease
• Hypoxia
• Pilocytic Astrocytoma
• Malignant Glioma
• Nervousness
• Hematologic Neoplasms
• Chromosomal Translocation

Pathways

• Methylation
• Pathogenesis
• Dna Methylation
• Tricarboxylic Acid Cycle
• Demethylation
• Glycolysis
• Histone Demethylation
• Localization
• Cell Growth
• Angiogenesis
• Dna Hypermethylation
• Oxidative Phosphorylation
• Histone Methylation

• Aging
• Regulation Of Gene Expression
• Cell Differentiation
• Mating
• Cell Proliferation
• Cell Development
• Metaphase

PTMs

• Methylation
• Demethylation
• Decarboxylation
• Carboxylation
• Reduction
• Deacetylation

• Phosphorylation
• Hydroxylation
• Nitration
• Cleavage
• Acetylation
• Oxidation

Research Areas

• Epigenetics
• Hypoxia
• Lipid and Metabolism

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/IDH2

Best Uses Of The IDH2 Marker Antibody

If you've been searching for the most effective IDH2 antibodies You've come the right spot. Boster's IDH2 Marker antibody is tested on a variety of platforms using known positive and negative samples. This information is used by the company to determine the specificity of antibodies and affinity. Boster also rewards scientists who write the first reviews of its products with product credits. Apart from providing the highest quality product, Boster also rewards scientists across the globe for their contribution to scientific research.

IDH2 Marker

IDH2 is involved in, among other things in the production and utilization of glutathione. This chemical reaction plays a crucial role in many chemical reactions. In this study, the IDH2 inhibitor AG-221 was found to be effective in treatment of RR-AML due to IDH2 mutations. The IDH2 inhibitor was prepared from the triazine precursor chemical, and was designed to be bioavailable for oral use. Additionally the IDH2 inhibitor showed significant effects on the longevity of mice.

Comparing to other markers, IDH2 knockdown has a tendency to lower levels of AKG. This marker can be useful in identifying leukemia cells that express IDH2. It is also possible to detect leukemia cells expressing IDH2 by using this marker. This study has demonstrated that knockdown of IDH2 leads to a marked increase of the a-KG level in tumor tissue.

The biology of cancer is affected by IDH2 mutations. The IDH2 mutation protein hinders the differentiation and maturation primitive cells. IDH2 mutations that block IDH2 could be a promising new treatment for certain types of cancer. To better understand the biological function of IDH2 in tumorigenesis, more research is needed. Further research on the IDH2 mutation is required to provide valuable information that can help doctors better treat cancer patients.

IDH2 mutations are also associated with resistance to AML treatment. Patients with this mutation have a lower chance of getting a C or even a C. This inability to treat could be explained through a predictive analysis of the mutations in other genes. The mutation of R172 in IDH2 results in increased expression of ID1 and ABCB1 genes. The IDH2 mutations in the gene R172 and R172 result in downregulation of genes KYNU, SUCLG2 and CD93 that regulate phagocytosis in apoptotic cells.

C-Myc, an oncogene, plays a key role in the process of metabolism and in cancer cell growth. The knockdown of the IDH2 wt-IDH2 decreased the protein and mRNA levels. C-Myc protein and mRNA levels were significantly lower in IDH2-shRNA-treated cells compared to control-transfected cells. The forced overexpression of wt–IDH2 raised the levels of cMyc protein a variety of cancer tissues.

Numerous cancers have had IDH2 mutations. Certain tumors have high-frequency mutations, like Chondrosarcoma or glioma. These findings suggest that IDH mutations could be a crucial marker to determine the genetic origin of cancer. Furthermore, IDH mutations are associated with the tumor's microenvironment. It is also a useful tool to treat patients suffering from cancer.

In a separate study researchers discovered that IDH2 expression was associated with C-MYC-mRNA expression in AML cell. The cBioPortal database showed that IDH2 knockdown reduced the expression of Bcl-2 (another survival molecule known for being controlled by C-MYC). This finding is further confirmed by RT-qPCR analysis of multiple targets of the c-Myc gene.

IDH2 mutations

IDH mutations are found in the majority of patients suffering from gliomas. These mutations affect the progenitors cells in their ability to differentiate into lineages. As a result, IDH mutations may promote tumorigenesis through interfering with the ability of cells to differentiate. These mutations can also cause hypermethylation, which can encourage tumor growth.

Arginaine 132 is the most frequently used location for IDh2 or IDH2 mutations. These mutations can cause substitutions and are most common in the catalytic pockets. R132H,R132C,R132L, and R132S are the most common substitutions. Both types of mutations could be mutually exclusive. However they can occur simultaneously. One example is the genetic connection between IDh2 and IDH2 mutations. A patient suffering from one type of mutation might not be affected by another.

IDH2 inhibitors show efficacy in preclinical models of acute myeloid leukemia. Furthermore, preclinical studies on IDH inhibitors have revealed that they inhibit mutant IDh2/2 functions. The drug also induces responses to MPN cells that express JAK2/STAT. In in vivo studies, it has been proven to possess anti-angiogenic qualities, but it isn't completely safe.

The mice in these studies had higher numbers of myeloid progenitor cell. The numbers of these cells were greater in patients with IDh2Mut. Mice with IDH2 mutations had higher numbers of meeloid cells CD16/32/34+. These cells are precursors for various types of leukemia. However, they aren't clonal. As such, they are more common for adults than for children.

A study of 21 patients suffering from IDH mutations found that the number of IDH2 mutations was much greater than was previously thought. One-fourth (24 percent) of patients suffering from IDH2-mutated myeloid cancer had IDh2 or IDH2 mutations. A fifth patient also had both IDh2 and IDH2 mutations. According to the authors, this omission es of mutdue to the absence of highly sensitive sequencing assays.

IDh2R132H and IDH2 mutations have a neomorphic effect on 2HG production. Both mutations don't cause glutamine metabolism that is reductive. While the mutants are tolerant to inhibitors, inhibition of the IDh2 mutation did not reverse the metabolic character. The loss of heterozygosity can be associated with higher levels of 2HG accumulation. This loss of heterozygosity does seem to be the reason for tumorigenesis.

Another study of Boster Bio's IDH2 mutants discovered that a majority of patients harbor both IDh2 and IDH2 mutations. The mutations were found in the same hot spot esdon 140, which is interesting. Furthermore, SNAPSHOT NGS performed on the samples failed to detect mutations in other genes. This results suggest that both IDH2 and IDh2 mutations are connected to BCR-A.

Premalignant solid tumors can be caused by IDH mutations. A subset of enchondromas has been linked to IDH mutations. These tumors can progress to chondrosarcomas. These cancers are sensitive to alkylating agents. Therefore, it is crucial to identify BCR-ABL mutated patients and treat them accordingly.

IDH2 inhibitors

In recent years, research has revealed a variety of interactions between IDh2 and IDH2 inhibitors, enabling the development of new therapeutic strategies. Many of these interactions are evident in BCL-2 which interacts with caspases, BAX and BIM. These triggers cause apoptosis. The Krebs cycle and convergence are also affected by the IDh2/2 isoforms. Other interactions are based on the TCA pathway and DNA methylation. Venetoclax also targets BCL-2 in order to increase the effectiveness of vaccination in gliomas with MUT/IDH.

These inhibitors may inhibit IDH2 activity by targeting FLT3 which is responsible for triggering biochemical phosphorylation events. By blocking IDH2 from interacting with the phosphodiesterase enzymethey can reduce 2-HG in cancer cells. This is a significant step towards more efficient treatments for cancer. It is worth noting that there are some questions that need to be addressed.

These inhibitors do not only inhibit IDh2 but also enhance IDh2 inhibition. The combination of these drugs has proven to have better clinical outcomes. It has been proven to be effective for patients who were recently diagnosed with AML with IDh2 mutation. The patients that suffer from this mutation comprise approximately 15% to 20% of all patients suffering from AML. Enasidenib and Idhifa have a 50% overall response rate when taken in isolation. However, a small percentage of patients develop resistance to these two medications and might require chemotherapy.

In the U.S., approximately 700 to 1,100 patients have IDh2 mutations. Agios and Celgene collaborated in 2010 to create a drug known as Idhifa. It's priced between $26,115 and $30 million per month, which the company says sho of generate $300 million in the U.S. at peak. The drug was also approved with a black box warning. However doctors are aware of this warning. It is likely to have an extremely high market share and co of also be used to treat other ailments.