CD123 inhibitors(Interleukin-3 receptor subunit alpha inhibitors), CD3 inhibitors(T cell surface glycoprotein CD3 inhibitors), FLT3 inhibitors(Tyrosine-protein kinase receptor FLT3 inhibitors)

Therapeutic Areas

NeoplasmsHemic and Lymphatic Diseases

Active Indication-

Inactive Indication

Hematologic Neoplasms

Originator Organization

ImClone LLC

Active Organization-

Inactive Organization

ImClone LLC

Drug Highest PhasePendingPreclinical

First Approval Date-

Regulation-

Structure

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100 Clinical Results associated with Anti-FLT3 radioimmunoconjugates(Eli Lilly and Company)

100 Translational Medicine associated with Anti-FLT3 radioimmunoconjugates(Eli Lilly and Company)

100 Patents (Medical) associated with Anti-FLT3 radioimmunoconjugates(Eli Lilly and Company)

Literatures (Medical) associated with Anti-FLT3 radioimmunoconjugates(Eli Lilly and Company)

01 Jan 2024·Free radical biology & medicine

Development of tandem antigen capture ELISAs measuring QSOX1 isoforms in plasma and serum

Article

Author: Ho, Thai ; Wan, Zijian ; Wang, Shaopeng ; Lake, Douglas ; Koelbel, Calvin ; Ruiz, Yvette

QSOX1 is a sulfhydryl oxidase that has been identified as a potential biomarker in multiple cancer types as well as acute decompensated heart failure. Three anti-QSOX1 monoclonal antibodies (mAbs) were generated: 2F1, 3A10, and 56-3. MAbs 2F1 and 3A10 were generated against the short isoform of recombinant QSOX1 (rQSOX1-S), and mAb 56-3 was generated against a peptide (NEQEQPLGQWHLS) from the long isoform of QSOX1 (QSOX1-L). Using these mAbs, tandem antigen capture ELISAs were developed to quantify both short and long isoforms of QSOX1 (Total QSOX1 ELISA) and QSOX1-L (QSOX1-L ELISA) in serum and plasma samples. The Total QSOX1 ELISA pairs mAbs 2F1 and 3A10 and has a limit of detection of 109.5 pM, while the QSOX1-L ELISA pairs mAbs 2F1 and 56-3 and has a limit of detection of 10 pM. The levels of total QSOX1 and QSOX1-L were measured in a cohort of paired sera and plasma from 61 donors ≥40 years old and 15 donors <40 years old. No difference in QSOX1 levels was detected between QSOX1-L and QSOX1-S in serum, but the mean concentration of QSOX1-L was found to be 3.21 nM in serum and 5.63 nM in plasma (**p = 0.006). Our tandem ELISAs demonstrate the wide range of concentrations of QSOX1-L and QSOX1-S among individual serum and plasma samples. Since the epitope of mAb 2F1 was mapped to the first CxxC motif at residues C70 and C73 and mAb 56-3 was generated against NEQEQPLGQWHLS in QSOX1-L, our findings support previous research which suggested that QSOX1-L is secreted from cells despite a putative transmembrane domain. The ELISAs reported here may be a useful tool for investigating QSOX1 isoforms as potential biomarkers in cancer and/or heart failure.

01 Jul 2023·International journal of biological macromolecules

Identification of an immunodominant neutralizing epitope of porcine Deltacoronavirus spike protein

Article

Author: Yan, Qigui ; Chen, Rui ; Wen, Yiping ; Cao, Sanjie ; Wen, Yimin ; Du, Senyan ; Yu, Enbo ; Song, Daili ; Zhao, Qin ; Huang, Xiaobo ; Han, Xinfeng ; Liang, Yixiao ; Wu, Rui ; Yang, Junpeng

Porcine deltacoronavirus (PDCoV) is a novel swine enteropathogenic coronavirus that, because of its broad host range, poses a potential threat to public health. Here, to identify the neutralizing B-cell epitopes within the S1-CTD protein, we generated three anti-PDCoV monoclonal antibodies (mAbs). Of these, the antibody designated 4E-3 effectively neutralized PDCoV with an IC50 of 3.155 μg/mL. mAb 4E-3 and one other, mAb 2A-12, recognized different linear B-cell epitopes. The minimal fragment recognized by mAb 4E-3 was mapped to ²⁸⁰FYSDPKSAV²⁸⁸ and designated S^280-288, the minimal fragment recognized by mAb 2A-12 was mapped to ⁵⁰⁶TENNRFTT⁵¹³, and designated S^506-513. Subsequently, alanine (A)-scanning mutagenesis indicated that Asp²⁸³, Lys²⁸⁵, and Val²⁸⁸ were the critical residues recognized by mAb 4E-3. The S^280-288 epitope induces PDCoV specific neutralizing antibodies in mice, demonstrating that it is a neutralizing epitope. Of note, the S^280-288 coupled to Keyhole Limpet Hemocyanin (KLH) produces PDCoV neutralizing antibodies in vitro and in vivo, in challenged piglets it potentiates interferon-γ responses and provides partial protection against disease. This is the first report about the PDCoV S protein neutralizing epitope, which will contribute to research of PDCoV-related pathogenic mechanism, vaccine design and antiviral drug development.

01 Apr 2018·Clinical cancer research : an official journal of the American Association for Cancer ResearchQ1 · MEDICINE

Flt-3L Expansion of Recipient CD8α+ Dendritic Cells Deletes Alloreactive Donor T Cells and Represents an Alternative to Posttransplant Cyclophosphamide for the Prevention of GVHD

Q1 · MEDICINE

Article

Author: Gartlan, Kate H. ; Lane, Steven W. ; Degli-Esposti, Mariapia A. ; Brocker, Thomas ; Henden, Andrea S. ; Browne, Daniel J. ; Markey, Kate A. ; Smyth, Mark J. ; Kuns, Rachel D. ; Koyama, Motoko ; Minnie, Simone A. ; Cheong, Melody ; Belz, Gabrielle T. ; Steptoe, Raymond J. ; Hill, Geoffrey R. ; Robb, Renee J. ; Martins, J. Paulo

Abstract:

Purpose: Allogeneic bone marrow transplantation (BMT) provides curative therapy for leukemia via immunologic graft-versus-leukemia (GVL) effects. In practice, this must be balanced against life threatening pathology induced by graft-versus-host disease (GVHD). Recipient dendritic cells (DC) are thought to be important in the induction of GVL and GVHD.Experimental Design: We have utilized preclinical models of allogeneic BMT to dissect the role and modulation of recipient DCs in controlling donor T-cell–mediated GVHD and GVL.Results: We demonstrate that recipient CD8α+ DCs promote activation-induced clonal deletion of allospecific donor T cells after BMT. We compared pretransplant fms-like tyrosine kinase-3 ligand (Flt-3L) treatment to the current clinical strategy of posttransplant cyclophosphamide (PT-Cy) therapy. Our results demonstrate superior protection from GVHD with the immunomodulatory Flt-3L approach, and similar attenuation of GVL responses with both strategies. Strikingly, Flt-3L treatment permitted maintenance of the donor polyclonal T-cell pool, where PT-Cy did not.Conclusions: These data highlight pre-transplant Flt-3L therapy as a potent new therapeutic strategy to delete alloreactive T cells and prevent GVHD, which appears particularly well suited to haploidentical BMT where the control of infection and the prevention of GVHD are paramount. Clin Cancer Res; 24(7); 1604–16. ©2018 AACR.

News (Medical) associated with Anti-FLT3 radioimmunoconjugates(Eli Lilly and Company)

01 Aug 2022

·www.prnewswire.com

BridGene Biosciences names David Sperandio, Ph.D., as Head of Chemistry

SAN JOSE, Calif., Aug. 1, 2022 /PRNewswire/ -- BridGene Biosciences, Inc., a biotechnology company using a proprietary chemoproteomics technology to discover and develop small molecules for high value, traditionally undruggable targets, today announced that David Sperandio, Ph.D., a medicinal chemist with more than 20 years' experience, has joined the company as the Head of Chemistry. Dr. Sperandio, an inventor on 23 patents and author of 25 peer-reviewed publications, has extensive experience leading cross-functional teams from molecule discovery through IND filing. Dr. Sperandio will lead the BridGene chemistry team and supervise research into covalent chemistry, chemical proteomics and quantitative mass spectrometry as methods for identifying undruggable targets. Additionally, Dr. Sperandio will be responsible for advancing BridGene's internal pipeline of first-in-class drugs for hard-to-drug targets in oncology. BridGene co-founder and CEO Ping Cao, Ph.D., commented, "David's addition to our leadership team and the recent Series B financing deepen BridGene's capabilities for using IMTAC™ to discover new drugs for novel and traditionally undruggable targets. David's leadership and experience will help expand BridGene's library of molecules to identify as potential drug candidates as we aim to advance a pipeline of first-in-class drugs for these new targets." Dr. Sperandio most recently served as an Executive Director at Biomea Fusion, where he led the team that identified BMF-500, a potential best-in-class targeted covalent FLT-3 inhibitor for the treatment of acute myeloid leukemia. Prior to joining Biomea Fusion, Sperandio led a collaboration of R2M Pharma Inc. with Tenaya Therapeutics Inc., which discovered novel HDAC6 inhibitors for cardiovascular diseases and was key for the clinical development of TN-301, an experimental treatment for heart failure. Dr. Sperandio started his career at Celera Corp. and focused on the structure-guided discovery of covalent reversible serine-protease inhibitors. He later moved to Gilead Sciences Inc., where he led the chemistry team that discovered Alobresib (GS-5829), a novel BRD4 inhibitor for prostate cancer, and Presatorvir (GS-5806), the first small molecule RSV fusion inhibitor that reached the clinic and showed proof of concept in men. Dr. Sperandio commented, "I am excited to join BridGene at such a dynamic time for the company. 2022 has been a remarkable year so far, and I look forward to working closely with the management team to continue to drive the success of IMTAC™." Dr. Sperandio obtained his doctoral degree in Organic Chemistry from the University of Zurich and completed his postdoctoral research at Stanford University. About BridGene Biosciences BridGene is a biotechnology company focused on discovering and developing innovative small molecules that drug traditionally undruggable targets, providing new paths to treat diseases. By using its proprietary chemoproteomics platform, IMTAC™, BridGene can screen small molecules against proteins in live cells to discover drug candidates for high value and traditionally undruggable targets. For this purpose, BridGene takes advantage of its proprietary, diverse library of tagged, drug-like small molecules. The ultimate goal is to enable breakthrough small molecule drug discovery with expanded mechanisms to treat diseases with targets previously inaccessible to small molecules. The uniqueness of BridGene's technology allows it to perform IMTAC™ screening for both covalent and non-covalent molecules, target different amino acids and discover new targets for disease treatments by deconvoluting phenotypic screening hits. The company is advancing a diversified pipeline of first-in-class drugs for targets in multiple disease areas. For more information, visit . Contact Tiberend Strategic Advisors, Inc. Investors Jonathan Nugent +1-205-566-3026 [email protected] Media Bill Borden +1-732-910-1620 [email protected] Dave Schemelia +1-609-468-9325 [email protected] SOURCE BridGene Biosciences

CollaborateFirst in ClassSmall molecular drug

100 Deals associated with Anti-FLT3 radioimmunoconjugates(Eli Lilly and Company)

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Indication	Highest Phase	Country/Location	Organization	Date
Hematologic Neoplasms	Preclinical	US	ImClone LLC	-

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Anti-FLT3 radioimmunoconjugates(Eli Lilly and Company)

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