Drug Database
ES

estrogens (Cenestin / Bijuva, Barr)

✓ Approved

Teva Pharmaceutical Industries Ltd. · ESR1

What is estrogens?

estrogens is a therapeutic agent developed by Teva Pharmaceutical Industries Ltd.. It is approved for therapeutic indications via intravaginal or oral (po).

Drug Profile

Brand NamesCenestin, Bijuva, Barr
CompanyTeva Pharmaceutical Industries Ltd.
Molecular TargetESR1
RouteIntravaginal, Oral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Teva Pharmaceutical Industries Ltd.

Mechanism of Action

Molecular Targets

estrogens acts on 1 molecular target:

ESR1estrogen receptor 1 (ER, ESR)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

estrogens is developed for 3 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Reproductive system and breast disordersAtrophic vulvovaginitis✓ Approved
Surgical and medical proceduresHormone replacement therapy✓ Approved
Reproductive system and breast disordersMenopausal symptoms✓ Approved

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Achieving multi-site photoisomerization within a single π-conjugated scaffold while retaining luminescent functionality remains a formidable challenge, as electronic coupling between isomerizable units typically promotes intramolecular energy transfer that suppresses sequential switching, and the additional nonradiative pathways inherent to multiple isomerizable bonds further impede emissive behavior. Herein, we report a methine-bridged trithiophene bearing 2,6-dichlorophenyl substituents, in which two C═C double bonds embedded in a thienoquinoid framework undergo photoisomerization to afford three interconvertible geometrical isomers (ZZ, EZ, and EE). The steric constraint imposed by the ortho-chloro substituents suppresses nonradiative torsional relaxation, yielding a fluorescence quantum yield of 0.40 for the ZZ-isomer in cyclohexane, which decreases upon photoisomerization to the EZ- and EE-isomers-a significant enhancement over the corresponding derivative lacking ortho-substituents on the aryl groups, accompanied by a markedly reduced Stokes shift. The photostationary state composition varies systematically with the irradiation wavelength, primarily reflecting differences in the molar absorption coefficients of the three isomers, thereby enabling wavelength-selective multi-state control over isomer distributions inaccessible under thermodynamic equilibrium. Fluorescence lifetime measurements revealed isomer-dependent excited-state lifetimes, confirming that molecular geometry governs the photophysical properties within this conjugated framework. This study establishes a molecular design strategy for luminescent multi-state photoswitches applicable to multi-level optical information processing.

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The inherent insolubility and poor processability of conventional covalent organic frameworks (COFs) represent a formidable obstacle to their practical deployment. Herein, we present a molecular design paradigm that circumvents this limitation by using a nonplanar monomer featuring a sterically congested, double‑layer conjugated benzene ring to construct a soluble heat-triggered solubility COF (HTS-COF). This structure substantially enlarges the interlayer spacing and attenuates π-π stacking interactions, thereby conferring reversible heat‑triggered solubility without compromising crystallinity or structural integrity. The resultant HTS‑COF readily undergoes solution processing into uniform membranes and aerogels. Notably, under dynamic filtration, the HTS‑COF membrane achieves expeditious and highly efficient iodine sequestration from both aqueous and organic media, exhibiting outstanding rejection efficiency and cycling stability.

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Human cytomegalovirus (HCMV) infection is one of the most common and severe viral complications following allogeneic hematopoietic stem cell transplantation (allo-HSCT), significantly increasing the risk of graft-versus-host disease (GVHD) and non-relapse mortality. Letermovir, as the first inhibitor targeting the HCMV terminase complex, blocks the cleavage of viral DNA and its packaging into viral capsids, demonstrating remarkable efficacy in early post-transplant HCMV prophylaxis. It significantly reduces the incidence of clinically significant HCMV infection (csCMVi) and indirectly contributes to improved GVHD- and relapse-free survival. However, while the potent viral suppression of this treatment provides clinical benefits, it also limits viral antigen exposure, which leads to delays in the reconstitution of HCMV-specific T cells and NK cells and consquently the increased risk of late-onset HCMV reactivation after drug discontinuation. This may also be associated with an elevated risk of Epstein-Barr virus reactivation and post-transplant lymphoproliferative disease (PTLD). This review aims to systematically summarize the dual effects of letermovir in allo-HSCT and analyzes its pharmacological mechanisms, clinical efficacy, impact on immune reconstitution, and potential consequences. Furthermore, it explores individualized management strategies based on immune monitoring to provide a theoretical basis for optimizing clinical practice.

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Martin Hannah S HS, Lamb-Echegaray Isabel D ID, Huang Paul P, Shallow Lillian L et al.

Mycobacterium tuberculosis (Mtb) infection kills more people worldwide than any other pathogen. While the Bacille Calmette-Guérin (BCG) vaccine for Mtb has been widely used for over a century, it provides insufficient protection to eradicate this disease. One of our labs has recently established that a protein antigen (H1) can be combined with a STING pathway agonist to achieve strong protection against Mtb in mice, with performance that exceeds that of the BCG vaccine. However, its reliance on a synthetic cyclic dinucleotide (CDN) with relatively poor cell uptake requires higher dosing levels, thus increasing costs. To increase the efficiency of this vaccine and provide a delivery strategy that could also be used in humans, the H1 Mtb antigen and CDN adjuvant were conjugated to genome-free MS2 viral capsids that included cationic mutations to increase cell uptake. Specifically, the H1 antigen was conjugated to the external surface of MS2 using a tyrosinase-mediated oxidative coupling reaction, and the native STING agonist cGAMP was coupled to internal cysteine residues through a reductively cleavable disulfide linker. The resulting MS2-H1 and MS2-cGAMP conjugates were then co-delivered for three doses of vaccination in mice before exposure to Mtb. The MS2-based vaccine platform was observed to have comparable efficacy to the original H1/CDN formulation, but its enhanced uptake properties enabled 57-fold less CDN and 3-fold less H1 antigen. Additionally, this vaccine elicited immune responses that have been previously demonstrated to correlate with protection. The ability of the capsid shells to protect the CDN cargo during transport allowed enzymatically produced, and thus readily accessible, cGAMP to be used instead of more costly CDNs that require many synthetic steps. This, combined with the reduced overall amount of CDN and H1 that was required, could lower the production costs of future vaccines substantially. Finally, the ability of the capsid-based carriers to bypass the membrane transporters for CDNs suggests that this enhanced vaccination platform is likely to exhibit improved human efficacy in future studies.

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Autoimmune diseases, such as systemic lupus erythematosus (SLE), are underscored by dysregulated B cell function including the production of autoantibodies, skewed population ratios, and aberrant signaling. Given that the family of nuclear factor kappa B (NF-κB) transcription factors govern responses to stimuli, survival, differentiation, and so forth understanding the intricate regulatory network of NF-κB in B cell biology is paramount for unraveling treatments for B cell-linked autoimmune diseases. Here, we focus on a negative regulator of NF-κB signaling, A20 ( TNFAIP3 ), that deactivates NF-κB transcription factor translocation through the ubiquitination and deubiquitination of target proteins. Haploinsufficiency in A20 results in an autoimmune phenotype and mutations to A20 have been associated with SLE, suggesting implications to B cell function. To investigate the role of A20 in NF-κB in human B cells, we generated a TNFAIP3 knockout (KO) Raji cell line. Cells were stimulated with either anti-IgM or Resiquimod (R848) to activate distinct NF-κB signaling pathways. Using qRT-PCR, western blotting, and flow cytometry, we assessed differences in gene expression, protein production, and NF-κB activation. We observed key limitations in using Epstein-Barr virus transformed B cell lines to model inducible NF-κB signaling.

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