Developing reliable animal models can be time-consuming, complex, and difficult to control. Our saporin-based approach enables targeted elimination of specific cell populations, allowing you to create precise animal models for studying disease, behavior, and biological function—without the long timelines of traditional methods.
This approach has been widely used to generate models for neurological and disease-specific research, where selective removal of defined cell types is critical to understanding function and pathology.
Their study examined whether selective loss of inhibitory interneurons in the hippocampus was enough to trigger temporal lobe epilepsy with hippocampal sclerosis (TLE-HS+). Injection of stable substance P-saporin (SSP-SAP) into the hippocampus of rats, rapidly targeted and eliminated specific inhibitory neurons.
Within 4–6 days, the animals developed spontaneous seizures. Although these early seizures subsided, the frequency and duration of self-generated epileptiform events steadily increased over the following three months, demonstrating progressive epileptogenesis. The researchers also observed ongoing loss of hippocampal neurons (particularly in the CA1 and CA3 regions) and increasing astrogliosis, both hallmark features of hippocampal sclerosis seen in human TLE patients.
Overall, the findings show that selective disruption of hippocampal inhibitory circuitry is sufficient to initiate epilepsy and drive the development of pathological changes that closely resemble human temporal lobe epilepsy with hippocampal sclerosis.
Unlike other models of epilepsy, the SSP-SAP model (Cat. #IT-11) has very specific toxicity that does not cause early death in the animal. The animal will have a normal lifespan, continuing to experience seizures.
With our Animal Models, you can:
Selectively remove defined cell types in vivo
Model disease pathways and functional outcomes
Study behavioral and physiological changes
Accelerate research timelines with rapid model generation
Most models are ready in just 2 weeks, helping you move from hypothesis to data faster.
Memory loss is a common part of aging, but it varies greatly from person to person. Research shows that changes in the gut microbiome may play an important role in age-related cognitive decline. Certain gut bacteria, especially P. goldsteinii, increase with age and produce medium-chain fatty acids (MCFAs).
These bacterial products trigger inflammation in peripheral immune cells through a receptor called GPR84. The resulting inflammation disrupts signaling through the vagus nerve, reducing communication between the gut and the brain. Weakened gut–brain communication leads to reduced activity in the hippocampus, making it harder to form and store new memories.
The authors injected CCK–SAP and Blank-SAP (125 ng in 0.5 μl per ganglion) into the nodose ganglion of the vagus nerve to determine their role in cognitive decline.
The authors work suggests that in aged mice, memory could be improved by reducing P. goldsteinii, blocking GPR84 signaling, or restoring vagus nerve activity, suggesting new potential treatments for age-related memory loss.
Did you know that Advanced Targeting Systems offers a curated collection of 379 secondary antibodies? This expanded selection provides reliable, consistent performance across a wide range of research applications.
Whether performing immunofluorescence, immunohistochemistry, western blot, flow cytometry, or cell and tissue staining, we have the secondary antibody to support your work.
If you do not see the specific target, host species, or format you need, please reach out. We would be happy to help identify the right secondary antibody for your application.
We’re highlighting our ZAP antibody internalization kits and our line of secondary antibody saporin conjugates. We have given these products the moniker “ZAP” in place of saporin.
Our ZAP conjugates consist of a variety of secondary antibodies that allow a large number of targeting agents to be screened quickly and cost-efficiently for specificity, functional binding, internalization, and EC50 determination.
The conjugates are constructed using either species-specific secondary antibodies, or streptavidin (for use with biotinylated Targeting Agents), and they are chemically attached to Saporin, a potent plant ribosome-inactivating proteins.
This article by Marquez et al. showcases how our secondary conjugates can be used to screen antibodies and then from that choose the best candidate to create a custom conjugation.
PTGFRN is a cell-surface protein that is upregulated in certain cancer types, including head and neck and, notably, pediatric medulloblastoma, an aggressive cancer with limited therapeutic options. With the selection of the mouse monoclonal antibody 33B7, the authors identified PTGFRN as a potential therapy target, and were able to show that it is internalized by incubation with 33B7.
This episode highlights our pHast line of conjugates. pHast conjugates are one of our fastest tools to quantitatively test your primary antibody’s specificity, binding, and internalization, providing results in 1 day.
The pHast conjugate binds to your primary antibody via a secondary antibody cross-linked to a pH-dependent fluorescent reporter. This fluorescent reporter will increase intensity as the pH of its surroundings becomes more acidic, such as you would see on the inside of a cell.
We’re highlighting our secondary saporin conjugate, Streptavidin-ZAP, which is streptavidinylated saporin. It combines with your biotinylated material to make a targeted toxin.
Unlike a secondary antibody binding to a primary antibody, the bond between streptavidin and biotin is rapid, essentially non-reversible, unaffected by most extremes of pH, organic solvents or denaturing reagents. It is essentially the strongest known noncovalent biological bond between protein and ligand. Streptavidin-ZAP is very modular and works with biotinylated antibodies, peptides, growth factor, aptamers, anything that will recognize a cell surface receptor and can be biotinylated.
This is a publication using a Streptavidin-ZAP reacted with an antibody as the targeting agent.
The authors’ objective was to investigate whether CD206-positive macrophages in the meninges play a role in regulating nociception and pain hypersensitivity. They injected rats intrathecally with conjugate made with biotinylated anti-CD206 reacted with Streptavidin-ZAP and looked at the effects on responses in naïve rats versus ones that received a skin incision, after depletion of CD206+ macrophages.
Their results indicated that depleting CD206+ meningeal macrophages did not regulate basal responses in naïve rats of either sex. However, ablation of these cells after skin injury induced mechanical hypersensitivity in male rats and not in females. Thus, they were able to conclude, that in a sex-dependent manner, CD206-positive meningeal macrophages prevent the spread of pain hypersensitivity after a minor injury.
Today we’re highlighting one of our saporin conjugates, Kisspeptin-SAP. This is a tool for eliminating cells that express the human and sheep G-protein coupled receptor, GPR54.
Kisspeptin is a ligand to GPR54 and functions in the hypothalamus, placenta, liver, pancreas, adipose tissue, bone, and limbic regions which shows the importance it can play in diagnosis and treatment of various disorders. It is one of the neuropeptides that governs the reproductive endocrine axis by regulating neuronal activity and secretion of hypothalamic gonadotropin releasing hormone (GnRH). GnRH is released from the hypothalamus to act on the anterior pituitary triggering the release of luteinizing hormone (LH), and follicle stimulating hormone (FSH). These gonadotropic hormones lead to sexual maturation and gametogenesis.
This is a 2023 publication using a Kisspeptin-saporin conjugate.
The objective of the authors was to test the functional role of ovine KNDy neurons in pulse generation and identify the roles of nearby Kiss1 receptor (Kiss1R)-containing cells. They performed these tests using conjugates NKB-SAP and Kisspeptin-SAP.
The results showed that NKB-SAP ablated over 90% of the KNDy cells, while Kisspeptin-SAP lesioned about two-thirds of the Kiss1R population. This led to a significant decrease in LH pulse amplitude and altering LH pulse patterns. NK3-SAP increased the interpulse interval without affecting the regularity of LH pulses, whereas Kiss-SAP disrupted their regular hourly occurrence but not the interpulse interval.
These findings suggest that KNDy neurons are critical for GnRH pulse generation in ewes, while ARC Kiss1R cells support the amplitude and regularity of these pulses, possibly as part of a positive feedback loop involving GABA or glutamate.
Today we’re highlighting one of our saporin conjugates, Anti-CD117-SAP. This is a tool for depleting cells that express CD117, the tyrosine kinase growth factor receptor.
CD117 is expressed on hematopoietic stem cells, mast cells, and acute myeloid leukemia cells. Some of the areas where CD117 plays an essential role is in the regulation of cell survival and proliferation, hematopoiesis, stem cell maintenance and mast cell development, migration and function.
Allogeneic hematopoietic stem cell transplantation can cure genetic diseases such as severe combined immunodeficiency (SCID), but it’s associated with significant toxicities such as graft-versus-host disease (GvHD). Using a patients’ own gene-modified hematopoietic stem and progenitor cells (HSPCs) can eliminate the risk of GvHD, but the treatment relies on gene transfer using viruses and genotoxic conditioning which carries risks.
The authors describe how base-editing is an alternative means to correct genetic defects while engineered virus-like particles (eVLPs) can deliver the base-edited proteins without the risks seen with viral integration.
In conclusion, transplantation of HSPCs that have been repaired through eVLP-mediated base-editing with CD117-ADC conditioning successfully reversed the SCID phenotype in mice, and highlights a significant advancement in disease treatment without the current toxicities.
We are highlighting one of our saporin conjugates, Neurotensin-SAP — a tool for depleting cells that express the neurotensin receptor (NTSR).
Neurotensin is a 13-amino-acid peptide found in the brain and spinal cord and is released by the hypothalamus. It is synthesized as part of a larger precursor protein that also includes the related neuropeptide neuromedin N. Neurotensin affects pituitary hormone release, interacts with the dopaminergic system, and is involved in vasodilation and hypotension. It can also modulate pain perception where intrathecal neurotensin has also been shown to be anti-nociceptive.
The objective was to determine whether NTSR1-expressing enteropancreatic neurons mediate the glucose-lowering effects of dietary olive oil and neurotensin, and to characterize their physiological role in glucose homeostasis.
The authors unilaterally injected neurotensin-SAP into the nodose ganglia to ablate NTSR1-expressing vagal neurons.
In their study, they demonstrated that neurotensin improves glucose tolerance by activating NTSR1-expressing enteropancreatic neurons, which connect the gut and pancreas. Ablation or disruption of these neurons abolished the glucoregulatory effects of both neurotensin and olive oil, establishing their necessity and sufficiency in this pathway.
Cholinergic degeneration in the nucleus basalis of Meynert (NBM) is linked to cognitive impairment and gait dysfunction in Alzheimer’s and Parkinson’s disease. The idea of modeling cholinergic degeneration in an animal model could provide opportunities to study the physiological role of the NBM and lead to new therapeutics.
The authors used a custom-designed cranial chamber implanted to the skull of rhesus monkeys to guide the injection of ME20.4-SAP (IT-15) to deplete cholinergic neurons in the NBM.
After injection, the effects were monitored in vivo using positron emission tomography-computed tomography (PET-CT), which essentially uses small amounts of a radioactive tracer and a special camera and computer to evaluate organ and tissue functions.
Through this work, the authors described an approach that yielded reliable spatial accuracy and delivery of ME20.4-SAP into the NBM.
In conclusion, the selective lesioning of cholinergic neurons in the NBM via ME20.4-SAP offers a promising method to study the pathophysiology of NBM degeneration which can hopefully fuel efforts in creating new therapeutics.
