Drug Database
SY

synth conjugated estrogens (Enjuvia)

✓ Approved

Teva Pharmaceutical Industries Ltd. · ESR1

What is synth conjugated estrogens?

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

Drug Profile

Brand NamesEnjuvia
CompanyTeva Pharmaceutical Industries Ltd.
Molecular TargetESR1
RouteOral (PO)
StatusApproved

Mechanism of Action

Molecular Targets

synth conjugated estrogens acts on 1 molecular target:

ESR1estrogen receptor 1 (ER, ESR)
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Therapeutic Indications

synth conjugated 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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Fumarate-based copolyesters with long-term stability and temperature-gated enzymatic degradation.

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Designing polyesters that combine long-term storage stability with controlled enzymatic deconstruction remains a formidable challenge in sustainable polymer development. Herein, we report a fumarate-based copolyester platform, poly(butylene terephthalate-co-fumarate) (PBTFu), that achieves this balance through stereoelectronic and conformational control. PBTFu exhibits exceptional mechanical robustness (>33.5 MPa strength and 760% elongation) and superior gas and water-vapor barrier properties, while retaining macroscopic integrity and substantial mechanical performance after 20 months of ambient storage. Crucially, PBTFu displays a sharp "on/off" degradability switch: it remains inert to hydrolysis and Candida antarctica lipase B at 37 °C but undergoes rapid depolymerization by Humicola insolens cutinase (HiC) at 55 °C. Combined experimental and computational investigations elucidate the molecular basis: the conjugated fumarate moiety lowers carbonyl electrophilicity to confer intrinsic hydrolytic resistance, while HiC's open catalytic cleft and a temperature-driven conformational match enable efficient nucleophilic attack. This work establishes PBTFu as a promising platform that leverages stereoelectronic stabilization and conformational dynamics to achieve durable yet HiC-depolymerizable packaging materials, offering a viable strategy for balancing storage stability with controlled enzymatic deconstruction.

PubMedChemistry (Weinheim an der Bergstrasse, Germany)2026-07-17

Multi-state Photoswitching in Thienoquinoid-Based Fluorescent Trithiophenes.

Nishimura Rio R, Hecht Stefan S, Saito Shohei S, Yamashita Ken-Ichi KI

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.

PubMedJournal of immunology (Baltimore, Md. : 1950)2026-07-17

mTECs and B cells form a thymic microniche associated with B-cell licensing.

Martinez Ryan J RJ, Rivera-León Adrianna M AM, Nikolaeva Avrora A, Esposito Kelsey K et al.

Thymic B cells rely on T cells and type-III IFN (IFN-λ) signaling for class switch recombination and effective licensing as APCs, a process essential for their role in establishing central T-cell tolerance. IFN-λ is produced exclusively by a subset of medullary thymic epithelial cells (mTECs); however, the spatial layout between B cells and IFN-λ-producing mTECs remain unclear. Here, we studied the distribution of thymic B cells and IFN-λ+ mTECs, alongside other mTEC populations, to better understand the niche required for thymic B-cell licensing. Using 26 target multiplex immunofluorescence imaging of the thymus, we identified populations of naïve B cells, licensed B cells, plasmacytoid dendritic cells, plasma cells, mTECs, and mimetic mTECs within the thymus. Spatial analysis revealed licensed B cells closely interacted with both IFN-λ+ mTEC and GP2+ microfold mTECs, with transcriptional analysis predicting CCL20-CCR6-mediated B-cell interactions with microfold and IFN-λ+ mTECs. However, studies in CCR6-deficient mice showed CCR6-CCL20 interaction was not required for B-cell licensing. To further investigate the role of GP2+ microfold mTECs in B-cell licensing, we studied the NOD/ShiLtJ mouse model, which we confirmed to have a natural reduction in microfold mTECs. Interestingly, the thymic B cells in NOD mice demonstrated reduced licensing, which was attributed to reductions in IFN-λ receptor expression on thymic B cells. These data indicate that microfold mTECs modulate the capacity of thymic B cells to undergo IFN-λ-induced licensing.

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Yang Xinyu X, Zou Yingdi Y, He Ningning N

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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B/F/TAF in people with both HIV-1 and hepatitis B: outcomes from the ALLIANCE open-label extension phase.

Avihingsanon Anchalee A, Leong Chee Loon CL, Hung Chien-Ching CC, Kiertiburanakul Sasisopin S et al.

Data on bictegravir/emtricitabine/tenofovir alafenamide (B/F/TAF) in people with both HIV-1 and HBV are limited, particularly for treatment-experienced people. ALLIANCE was a randomized, double-blind, active-controlled, phase 3 study of B/F/TAF versus dolutegravir (DTG) + emtricitabine/tenofovir disoproxil fumarate (F/TDF) in treatment-naïve adults with HIV-1 RNA ≥ 500 copies/mL and HBV DNA ≥ 2000 IU/mL. Participants received continuous B/F/TAF through 144 weeks (≥ 96 weeks of blinded treatment plus 48-week optional open-label extension [OLE]) or switched to B/F/TAF after ≥ 96 weeks of DTG + F/TDF through 48 weeks of OLE. Here we report outcomes from the OLE. 121 participants were included in the continuous B/F/TAF group; 89 in the switch group. Median B/F/TAF exposure was 186.4 and 48 weeks, respectively. HIV-1 and HBV suppression rates (missing = excluded) were maintained in both groups (B/F/TAF Week 144: 99.0% and 80.2%; switch OLE Week 48: 95.4% and 86.6%, respectively). Both groups had improved alanine aminotransferase normalization. HBV envelope antigen loss and seroconversion occurred in 44.8% and 29.3%, respectively, of participants receiving continuous B/F/TAF (Week 144) and 17.0% and 12.8% in the switch group (OLE Week 48). HBV surface antigen loss and seroconversion occurred in 22.5% and 15.5% (continuous B/F/TAF), and 4.3% and 0% (switch group) of participants, respectively. One participant (continuous B/F/TAF) discontinued due to study drug-unrelated treatment-emergent adverse event. No treatment-emergent resistance was reported. B/F/TAF was effective in HIV-1 and HBV suppression and well tolerated in treatment-naïve individuals for ≤ 3 years and ≤ 1 year after switching from a TDF-based regimen. Trial registration ClinicalTrials.gov NCT03547908 (first registration 2018-05-24).

PubMedJournal of immunology (Baltimore, Md. : 1950)2026-07-17

Hidden effects of polymyxin B: Its role in activating TLR2-mediated inflammatory responses.

Goto Yoshikuni Y, Ogawa Yuko Y, Ogawa Kenji K, Ohnishi Atsushi A et al.

Polymyxins are cyclic cationic lipopeptide antibiotics that disrupt both the outer and inner membranes of Gram-negative bacteria. They also bind to bacterial lipopolysaccharides (LPSs), thereby inhibiting LPS recognition by Toll-like receptor 4 (TLR4) and preventing macrophage activation. However, the immunomodulatory effects of polymyxin B during infection, in which multiple host- and bacteria-derived factors coexist, remain unclear. In this study, we examined the impact of polymyxin B, a representative polymyxin antibiotic, on mouse macrophage responses in the presence of interferon γ (IFN-γ), with or without LPS stimulation. Polymyxin B induced nitric oxide (NO) production when macrophages were exposed to high concentrations of IFN-γ. In the presence of lower concentrations of IFN-γ, polymyxin B alone cannot induce NO production, but together with LPS can cause the induction of NO production. These NO productions were not largely affected by TLR4 deficiency but were attenuated when TLR2 was deficient. Furthermore, polymyxin B-immobilized agarose beads precipitated TLR2 from cell extracts, indicating an association between polymyxin B and TLR2. This association was not inhibited by LPS, although polymyxin B and LPS synergistically induced NO production. Collectively, these findings demonstrate that polymyxin B (together with LPS) associates with TLR2 and functions as a TLR2 agonist, suggesting that polymyxin B preparations can induce macrophage activation under conditions in which IFN-γ and LPS are present.

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