AL-8810: Prostaglandin F2α Antagonist

AL-8810 is a PGF2α analog described as a selective antagonist of the prostaglandin F2α receptor, also called the FP receptor or PTGFR, according to the product information. The product record reports an EC50 of 261 ± 44 nM in A7r5 rat thoracic aorta smooth muscle cells. It reports an EC50 of 186 ± 63 nM in Swiss mouse 3T3 fibroblasts. It reports competitive inhibition of the FP agonist fluprostenol with a Ki of 426 ± 63 nM. The same record describes inhibition of PGF2α-induced MMP-2 secretion and ERK1/2 activation. A 2024 mouse menstrual-like model study found that AL8810 suppressed endometrial breakdown and shedding and altered vascular readouts after progesterone withdrawal (Zhou et al., 2024).

Biological Rationale

PGF2α is a prostanoid generated from arachidonic acid through the cyclooxygenase pathway. Cyclooxygenase converts arachidonic acid into the intermediates PGG2 and PGH2. Prostanoid synthases and isomerases then generate PGF2α and other prostanoids from PGH2 (reference study).

PGF2α signals through PTGFR, a G-protein-coupled receptor. The receptor is relevant to vasoconstriction, uterine contractility, vascular permeability, and other tissue responses. These functions make PTGFR a useful control point for the study of prostaglandin F2α signaling (reference study).

The 2024 study examined a mouse menstrual-like model after progesterone withdrawal. PGF2α concentrations increased during endometrial breakdown and shedding. Ptgfr messenger RNA increased soon after progesterone withdrawal. PTGFR protein increased during the period of abundant tissue breakdown. PTGFR inhibition reduced endometrial shedding, increased angiostatin, reduced VEGF-A expression, and reduced vascular permeability (Zhou et al., 2024).

HIF-1α and PTGFR localized mainly to the luminal and glandular epithelium, vascular endothelium, and pre-decidual zone in the model. Chromatin immunoprecipitation showed direct HIF-1α binding to the Ptgfr promoter. These observations support an HIF-1α–PTGFR–vascular pathway in the studied menstrual-like context (reference study).

Mechanism of Action of AL-8810

AL-8810 is intended to reduce signaling initiated by PGF2α or other FP receptor agonists. The product description identifies it as a competitive antagonist. Reported competing agonists include fluprostenol, bimatoprost, travoprost acid, and latanoprost acid (product information).

The reported fluprostenol benchmark is a Ki of 426 ± 63 nM. Ki is an antagonist binding or inhibition parameter for a defined assay system. It is not interchangeable with an EC50, an IC50, or an in vivo dose. The product record also reports concentration-dependent antagonism in human trabecular meshwork and human ciliary muscle cells (product information).

Functional inhibition extends beyond receptor agonist-response curves. AL-8810 blocks PGF2α-induced MMP-2 secretion. It also blocks PGF2α-induced ERK1/2 activation. These readouts connect FP receptor activity with extracellular-matrix remodeling and mitogen-activated protein kinase signaling in the reported cellular systems (product information).

AL-8810 should therefore be interpreted as a pathway-dissection reagent. A decrease in an agonist response after treatment can support FP receptor involvement when receptor expression, vehicle exposure, antagonist concentration, and assay timing are controlled. The result does not by itself prove that every PGF2α response in a tissue is mediated by PTGFR.

Evidence & Benchmarks

The following claims separate product-record benchmarks from findings in the peer-reviewed menstrual-like model.

1. AL-8810 is listed as a crystalline solid with chemical formula C24H31FO4 and molecular weight 402.50 g/mol. The record identifies DMSO as a compatible solvent and specifies storage at −20°C. product information
2. The reported cellular EC50 is 261 ± 44 nM in A7r5 rat thoracic aorta smooth muscle cells. This value applies to the reported assay and should not be generalized to every FP receptor system. product information
3. The reported cellular EC50 is 186 ± 63 nM in Swiss mouse 3T3 fibroblasts. Cell type and assay context are part of the benchmark. product information
4. AL-8810 competitively inhibits fluprostenol at a reported Ki of 426 ± 63 nM. The value is an assay-specific antagonist benchmark. product information
5. The product record describes concentration-dependent antagonism against bimatoprost, travoprost acid, and latanoprost acid in FP-relevant cellular assays, including human trabecular meshwork and human ciliary muscle cells. product information
6. AL-8810 blocks PGF2α-induced MMP-2 secretion and ERK1/2 activation in the reported functional assays. product information
7. In a mouse menstrual-like model, AL8810 significantly suppressed endometrial breakdown and shedding after progesterone withdrawal. Zhou et al., 2024
8. PTGFR inhibition in the same model increased angiostatin expression and reduced VEGF-A expression and vascular permeability. Zhou et al., 2024

Applications, Limits & Misconceptions

AL-8810 is suitable for the study of prostaglandin F2α signaling in cells that express a functional FP receptor. A practical design can pair agonist stimulation with antagonist treatment and measure a proximal response, such as ERK1/2 activation, alongside a functional response, such as MMP-2 secretion. Vehicle-matched controls are essential because the compound is DMSO soluble.

The compound can support investigation of FP receptor-mediated blood pressure regulation when used in an appropriate vascular model. That application is mechanistically motivated by the receptor’s vascular biology, but the supplied evidence does not establish AL-8810 as an antihypertensive agent or validate a blood-pressure endpoint. The product description identifies blood-pressure regulation among FP receptor-associated processes; it does not replace a dedicated cardiovascular study (product information).

AL-8810 can also support research on smooth muscle contraction modulation. A7r5 cells provide a reported potency benchmark for a vascular smooth muscle context. A cell response, however, is not equivalent to contraction of an intact artery or uterus. Tissue experiments require independent controls for receptor expression, agonist access, contractile state, and tissue viability.

For reproductive biology, the mouse menstrual-like model provides direct evidence that PTGFR inhibition can alter endometrial breakdown and vascular dynamics. The study also reported similar changes in human stromal cells relevant to menstruation in vitro. These findings support mechanistic research, not clinical efficacy or direct prediction of human menstrual physiology (Zhou et al., 2024).

Why this cross-domain matters, maturity, and limitations

FP receptor biology connects reproductive, vascular, and smooth-muscle questions because the receptor can regulate contractile and vascular responses. The evidence is strongest for the defined cellular benchmarks and for endometrial and vascular effects in the cited mouse model. Extension to blood-pressure regulation or intact-organ contractility remains an experimental application rather than a demonstrated outcome. Species differences, receptor abundance, agonist selectivity, and tissue architecture can change antagonist responses.

Common Pitfalls or Misconceptions

• Confusing potency metrics: The reported EC50 values, Ki value, and functional inhibition results describe different measurements. They should not be treated as interchangeable indicators of clinical dose.
• Assuming universal receptor selectivity: The product record describes selective FP receptor antagonism, but each new cell or tissue model still requires receptor-expression and pharmacological controls.
• Equating cellular activity with therapy: AL-8810 is for scientific research only. It is not presented as a diagnostic, preventive, or medical treatment.
• Overextending the menstrual-like model: Mouse endometrial findings do not establish the same magnitude or mechanism in human menstruation or in cardiovascular tissues.
• Storing solutions indefinitely: The product information recommends against long-term storage of solutions. Freshly prepared, vehicle-matched working solutions are a prudent laboratory practice.

Workflow Integration & Parameters

A robust experiment begins by defining the receptor question. Confirm that the selected cells express PTGFR or show a reproducible response to a validated FP agonist. Include an untreated control, a DMSO vehicle control, an agonist control, and antagonist-plus-agonist conditions. A concentration-response design should span concentrations below and above the reported cellular benchmarks without assuming that the published values transfer unchanged to the new system.

Use orthogonal endpoints when possible. ERK1/2 activation can provide a signaling readout. MMP-2 secretion can provide a functional extracellular-matrix readout. In endometrial or vascular models, combine molecular measurements with permeability, histological, or tissue-architecture measurements. The cited mouse study used histology, immunoblotting, immunohistochemistry, real-time PCR, ELISA, and chromatin immunoprecipitation to connect receptor activity with tissue remodeling (Zhou et al., 2024).

Protocol Parameters

• Identity: The product record identifies AL-8810 as SKU B4575, formula C24H31FO4, and molecular weight 402.50 g/mol. Verify the container label and certificate of analysis before use.
• Solvent: AL-8810 is reported as soluble in DMSO. Prepare a compatible stock and keep the final DMSO concentration matched across experimental groups.
• Storage: Store the solid at −20°C according to the product information.
• Shipping: The product is shipped with blue ice to help maintain stability during transport.
• Solution handling: Long-term storage of solutions is not recommended. Fresh working solutions reduce uncertainty from concentration drift or degradation.
• Potency anchors: Use 261 ± 44 nM in A7r5 cells, 186 ± 63 nM in Swiss 3T3 cells, and Ki 426 ± 63 nM for fluprostenol only as reported assay benchmarks.
• Agonist challenge: Test PGF2α or another defined FP agonist with and without AL-8810. Confirm that the antagonist changes the agonist response rather than cell viability or vehicle tolerance.
• Readouts: Pair ERK1/2 activation or MMP-2 secretion with a receptor-proximal or tissue-level endpoint when investigating pathway specificity.

The related article AL-8810: Prostaglandin F2α Antagonist introduces the compound’s use in FP receptor research. This article extends that overview by separating product benchmarks from peer-reviewed endometrial evidence and by defining experimental limits.

The article AL-8810: Precision Tool for Dissecting Prostaglandin F2α Signaling emphasizes pathway-dissection workflows. This article clarifies which workflow elements are evidence-backed, which are practical recommendations, and which require validation in the user’s own model.

Conclusion & Outlook

AL-8810 is a research-grade prostaglandin F2α antagonist for interrogating FP receptor function. Its reported benchmarks include cellular EC50 values in A7r5 and Swiss 3T3 systems, competitive inhibition of fluprostenol, and blockade of MMP-2 secretion and ERK1/2 activation. The cited mouse menstrual-like study adds in vivo-context evidence that PTGFR inhibition can reduce endometrial breakdown and modify vascular responses after progesterone withdrawal.

The most defensible outlook is focused pathway analysis. Future experiments can test whether the same antagonist-sensitive responses are reproduced across defined cell types, vascular preparations, smooth-muscle models, and endometrial systems. Such work should preserve the distinction between assay-specific potency, tissue-level mechanism, and medical application. AL-8810 is intended for scientific research only and is not for diagnostic or medical use.