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概览

疾病领域	数量

肿瘤	1

排名前五的药物类型	数量

治疗性疫苗	1
类毒素疫苗	1

关联

10

项与 International Centre for Genetic Engineering and Biotechnology (ICGEB) 相关的药物

Heberprovac

靶点-

作用机制

免疫刺激剂

在研机构

International Centre for Genetic Engineering and Biotechnology (ICGEB)

原研机构

International Centre for Genetic Engineering and Biotechnology (ICGEB)

在研适应症

前列腺癌

非在研适应症-

最高研发阶段临床2期

首次获批国家/地区-

首次获批日期-

CIGB-500

靶点

GHR

作用机制

GHR激动剂

在研机构

Centro de Ingenieria Genetica y Biotecnologia

原研机构

Centro de Ingenieria Genetica y Biotecnologia

在研适应症

心肌梗塞

非在研适应症

脑缺血

最高研发阶段临床1/2期

首次获批国家/地区-

首次获批日期-

Hebervis

靶点

EGFR

作用机制

EGFR拮抗剂

在研机构-

原研机构

International Centre for Genetic Engineering and Biotechnology (ICGEB)

在研适应症-

非在研适应症

溃疡性结肠炎 [+1]

最高研发阶段终止

首次获批国家/地区-

首次获批日期-

100 项与 International Centre for Genetic Engineering and Biotechnology (ICGEB) 相关的临床结果

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0 项与 International Centre for Genetic Engineering and Biotechnology (ICGEB) 相关的专利（医药）

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140

项与 International Centre for Genetic Engineering and Biotechnology (ICGEB) 相关的文献（医药）

2024-07-01·Nature Immunology

Cell shape sensing licenses dendritic cells for homeostatic migration to lymph nodes

Article

作者: Fusilier, Zoé ; Gratia, Matthieu ; Alraies, Zahraa ; Legoix, Patricia ; Lacerda Mariano, Livia ; Benvenuti, Federica ; Manel, Nicolas ; Ginhoux, Florent ; Williart, Alice ; Calmettes, Vincent ; Sáez, Pablo J ; P F Nader, Guilherme ; Maria Piperno, Giulia ; Moreau, Aurélie ; Maurin, Mathieu ; Yatim, Aline ; Dunsmore, Garett ; Le Dorze, Anne-Louise ; Rivera, Claudia A ; Delgado, Maria-Graciela ; Amadio, Roberto ; Popard, Henri ; Sanséau, Doriane ; Dejean, Anne S ; Lawrence, Toby ; Lennon-Duménil, Ana-Maria ; Kniazeva, Anna ; Lamiable, Olivier ; Nakano, Hideki ; Crestey, Lou ; Cook, Donald N ; Piel, Matthieu ; Albaud, Benoit ; Moreau, Hélène D

AbstractImmune cells experience large cell shape changes during environmental patrolling because of the physical constraints that they encounter while migrating through tissues. These cells can adapt to such deformation events using dedicated shape-sensing pathways. However, how shape sensing affects immune cell function is mostly unknown. Here, we identify a shape-sensing mechanism that increases the expression of the chemokine receptor CCR7 and guides dendritic cell migration from peripheral tissues to lymph nodes at steady state. This mechanism relies on the lipid metabolism enzyme cPLA2, requires nuclear envelope tensioning and is finely tuned by the ARP2/3 actin nucleation complex. We also show that this shape-sensing axis reprograms dendritic cell transcription by activating an IKKβ–NF-κB-dependent pathway known to control their tolerogenic potential. These results indicate that cell shape changes experienced by immune cells can define their migratory behavior and immunoregulatory properties and reveal a contribution of the physical properties of tissues to adaptive immunity.

2024-06-03·Brain

Mitigation of TDP-43 toxic phenotype by an RGNEF fragment in amyotrophic lateral sclerosis models

Article

作者: Szabla, Robert ; Lyons, Taylor A ; Kaplanis, Brianna ; Junop, Murray ; Buratti, Emanuele ; Strong, Michael J ; Withers, Benjamin ; Noches, Veronica ; Droppelmann, Cristian A ; Campos-Melo, Danae ; McLellan, Crystal ; Sonkar, Kirti S ; Simon, Anne ; Kramer, Jamie M ; Amzil, Hind

AbstractAggregation of the RNA-binding protein TAR DNA binding protein (TDP-43) is a hallmark of TDP-proteinopathies including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). As TDP-43 aggregation and dysregulation are causative of neuronal death, there is a special interest in targeting this protein as a therapeutic approach. Previously, we found that TDP-43 extensively co-aggregated with the dual function protein GEF (guanine exchange factor) and RNA-binding protein rho guanine nucleotide exchange factor (RGNEF) in ALS patients. Here, we show that an N-terminal fragment of RGNEF (NF242) interacts directly with the RNA recognition motifs of TDP-43 competing with RNA and that the IPT/TIG domain of NF242 is essential for this interaction.Genetic expression of NF242 in a fruit fly ALS model overexpressing TDP-43 suppressed the neuropathological phenotype increasing lifespan, abolishing motor defects and preventing neurodegeneration. Intracerebroventricular injections of AAV9/NF242 in a severe TDP-43 murine model (rNLS8) improved lifespan and motor phenotype, and decreased neuroinflammation markers.Our results demonstrate an innovative way to target TDP-43 proteinopathies using a protein fragment with a strong affinity for TDP-43 aggregates and a mechanism that includes competition with RNA sequestration, suggesting a promising therapeutic strategy for TDP-43 proteinopathies such as ALS and FTD.

2024-02-01·eBioMedicine

Reactivation of Kaposi’s sarcoma-associated herpesvirus (KSHV) by SARS-CoV-2 in non-hospitalised HIV-infected patients

Article

作者: Blumenthal, Melissa J ; Schäfer, Georgia ; Lambarey, Humaira ; Jennings, Lauren ; Joyimbana, Wendy ; Orrell, Catherine ; Chetram, Abeen

BACKGROUNDWhile acute SARS-CoV-2 infection and associated inflammation resulted in substantial morbidity and mortality during the COVID-19 pandemic, particularly in unvaccinated patients, long-term effects of SARS-CoV-2 exposure for reactivation of latent oncogenic herpesviruses, such as KSHV, is unknown.METHODSWe performed a longitudinal observational cross-sectional study on 407 non-hospitalised adult HIV-infected (CD4 count <350 cells/μL) patients attending antiretroviral therapy services in Gugulethu, South Africa, from October 2020 to April 2023.FINDINGSKSHV seroprevalence was 53.5%; the quarterly SARS-CoV-2 seroprevalence increased from 76.2% (before roll-out of COVID-19 vaccinations) to 94.9%, with 32.2% being self-reportedly vaccinated against COVID-19. Over the course of recruitment, the quarterly percentage of patients with detectable KSHV viral load (VL) in the peripheral blood increased from 3.3% to 69.2%. The presence of KSHV VL was significantly associated with SARS-CoV-2 RBD antibody titers in unvaccinated (median RBD IgG OD 1.24 [IQR 0.82-2.42] in non-reactivated versus 2.83 [IQR 1.08-4.72] in reactivated patients, p = 0.0030) but not in vaccinated patients (median RBD IgG OD 5.13 [IQR 4.11-6.36] in non-reactivated versus 4.53 [IQR 2.90-5.92] in reactivated patients, p = 0.086). Further logistic regression revealed significantly higher odds of KSHV reactivation in unvaccinated, previously SARS-CoV-2 exposed patients (p = 0.015, adjusted OR 1.28 [95% CI: 1.05-1.55]), but not vaccinated patients (p = 0.080, adjusted OR 0.83 [95% CI: 0.67-1.02]). Interestingly, detectable KSHV VL was not associated with increased inflammatory markers such as C-reactive protein and interleukin-6.INTERPRETATIONHigh, and most likely repeated, exposure to SARS-CoV-2 in unvaccinated individuals may have long-term consequences for reactivation of KSHV infection as shown here in the context of HIV-infected patients with impaired immune functions. Post-pandemic prevention and/or monitoring strategies of potential KSHV-associated pathologies in high-risk patients with immunodeficiencies are therefore highly recommended.FUNDINGThis research was funded by the EDCTP2 programme (Training and Mobility Action TMA2018SF-2446).

100 项与 International Centre for Genetic Engineering and Biotechnology (ICGEB) 相关的药物交易

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100 项与 International Centre for Genetic Engineering and Biotechnology (ICGEB) 相关的转化医学

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临床2期

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当前项目

药物(靶点)	适应症	全球最高研发状态

Heberprovac	前列腺癌更多	临床2期
JAIVAC-1	恶性疟更多	终止
Hebervis ( EGFR )	口腔炎更多	终止
Abdala ( SARS-CoV-2 S protein )	新型冠状病毒感染更多	无进展
CIGB-550-E7	宫颈癌更多	无进展