DNA intercalators, NF-κB inhibitors(Nuclear factor NF-kappa-B complex inhibitors), SSRP1 inhibitors(Structure specific recognition protein 1 inhibitors)

+ [3]

Therapeutic Areas

NeoplasmsRespiratory DiseasesSkin and Musculoskeletal Diseases

Active Indication

Lung CancerMelanoma

Inactive Indication-

Originator Organization

Cleveland BioLabs, Inc.

Active Organization

Cleveland BioLabs, Inc.

Roswell Park Comprehensive Cancer Center

Inactive Organization

Statera Biopharma, Inc.

Drug Highest PhasePreclinical

First Approval Date-

Regulation-

Structure

Molecular FormulaC23H27ClN2O2

InChIKeyJURGRPIWKHUHSL-UHFFFAOYSA-N

CAS Registry1197397-96-8

100 Clinical Results associated with CBL 0175(Incuron)

100 Translational Medicine associated with CBL 0175(Incuron)

100 Patents (Medical) associated with CBL 0175(Incuron)

Literatures (Medical) associated with CBL 0175(Incuron)

01 Sep 2023·BioEssays : news and reviews in molecular, cellular and developmental biology

The survival of curaxins in the cancer arena.

Article

Author: Papaspyropoulos, Angelos ; Theocharous, Giorgos ; Gorgoulis, Vassilis

With DNA damage being a primary anti-cancertarget, a need has arisen for the development of an approach that is a harmlessfor normal tissues but allows for cancer cell-specific cytotoxicity. Previous researchfrom K. Gurova's suggests that small compounds, namely curaxins that bind theDNA can cause chromatin instability and cell death in a cancer cell-specificmanner. In this brief perspective commentary, we investigate how the scientificcommunity has further developed this anti-cancer approach.

13 Apr 2022·Journal of Healthcare EngineeringQ4 · MEDICINE

The Current Status of SSRP1 in Cancer: Tribulation and Road Ahead

Q4 · MEDICINE

ReviewOA

Author: Peng, Liping ; Wang, Lihui ; Jia, Shengnan ; Zhang, Ling ; Guo, Baofeng

Background and Objectives. Owing to the complexity and heterogeneity of tumors, cancer’s early diagnoses and treatment have become a provocation. Structure-specific recognition protein-1 (SSRP1) is a histone (H3-H4 or H2A-H2B) chaperone in chromatin-related processes such as transcription, cell cycle control, and DNA replication, reported in various tumor tissues. It may also be used as a biomarker. This study aimed to highlight the role of SSRP1 in cancer with a focus on the current progress and future perspective. Methods. We search PubMed and Web of Sciences with keywords “SSRP1” and “Cancer.” Only English literature was included, and conference papers and abstract were all excluded. Results. Transcription factors are classified into three groups based on their DNA binding motifs: simple helix-loop-helix (bHLH), classical zinc fingers (ZF-TFs), and homeodomains. The tumor-suppressive miR-497 (microRNA-497) acted as an undesirable regulator of SSRP1 upregulation, which led to tumor growth. The siRNA (small interfering RNA) knockdown of SSRP1 hindered cell proliferation along with incursion and glioma cell migration. Through the AKT (also known as protein kinase B) signaling pathway, SSRP1 silencing affected cancer apoptosis and cell proliferation. Conclusion. The MAPK (mitogen-activated protein kinase) signaling pathway’s phosphorylation was suppressed when SSRP1 was depleted. The effect of curaxins on p53 and NF-B (nuclear factor-κB), and their toxicity to cancer cells, is attributable to the FACT (facilitates chromatin transcription) complex’s chromatin trapping.

01 Jan 2022·DNA Repair

The FAcilitates Chromatin Transcription (FACT) complex: Its roles in DNA repair and implications for cancer therapy

Review

Author: Ray, Sutapa ; Bhakat, Kishor K

Genomic DNA in the nucleus is wrapped around nucleosomes, a repeating unit of chromatin. The nucleosome, consisting of octamer of core histones, is a barrier for several cellular processes that require access to the naked DNA. The FAcilitates Chromatin Transcription (FACT), a histone chaperone complex, is involved in nucleosome remodeling via eviction or assembly of histones during transcription, replication, and DNA repair. Increasing evidence suggests that FACT plays an important role in multiple DNA repair pathways including transcription-coupled nucleotide excision repair (TC-NER) of UV-induced damage, DNA single- and double-strand breaks (DSBs) repair, and base excision repair (BER) of oxidized or alkylated damaged bases. Further, studies have shown overexpression of FACT in multiple types of cancer and its association with drug resistance and patients' poor prognosis. In this review, we discuss how FACT is accumulated at the damage site and what functions it performs. We describe the known mechanisms by which FACT facilitates repair of different types of DNA damage. Further, we highlight the recent advances in a class of FACT inhibitors, called curaxins, which show promise as a new adjuvant therapy to sensitize multiple types of cancer to chemotherapy and radiation.

100 Deals associated with CBL 0175(Incuron)

R&D Status

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Lung Cancer	Preclinical	US	Cleveland BioLabs, Inc.	15 Apr 2010
Lung Cancer	Preclinical	US	Roswell Park Comprehensive Cancer Center	15 Apr 2010
Melanoma	Preclinical	US	Cleveland BioLabs, Inc.	15 Apr 2010
Melanoma	Preclinical	US	Roswell Park Comprehensive Cancer Center	15 Apr 2010
Solid tumor	Preclinical	US	Statera Biopharma, Inc.	-

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