# Welcome ## About Aubrai is the world’s first decentralized scientific agent with knowledge stemming from thousands of private lab notes, internal chats and unpublished insights from the lab of Dr. Aubrey de Grey and the collective intelligence of the global longevity community. Co-developed by VitaDAO and BIO, the first BioAgent is designed to fight the greatest killer of all time: Aging. As an onchain AI co-scientitst, Aubrai can generate and validate hypotheses, design wet-lab experiments and encrypt data when asked, enriching research outputs while protecting trade secrets. At the heart of Aubrai's mission lies the Robust Mouse Rejuvenation ([RMR2](broken://spaces/JVEd82UmRFcSrucl82Qv)) project – Aubrey's ambitious study to double the remaining lifespan of middle‑aged mice. If successful, it could be aging's "AlphaFold moment": a proof that multi‑target rejuvenation works and is worth scaling. ## Architecture Overview Aubrai is built on the [BioAgents](https://github.com/bio-xyz/bioagents) framework powered by [ElizaOS](https://github.com/elizaOS/eliza) and purpose-built for longevity science. It layers domain-specific prompts / tools and curated longevity literature on top of the BioAgents framework. Because BioAgents is under active development, Aubrai continuously inherits upstream improvements, while adding domain-specific upgrades. This approach ensures Aubrai's intelligence capabilities compound and grow with every release. Aubrai extends core components from the BioAgents framework, optimized for the domain of longevity research. Its key intelligence building blocks: * Internal knowledge * Longevity knowledge graph * OpenScholar fine-tuned on longevity literature #### Internal Knowledge Aubrai has been trained on a private collection of documents from the [LEV Foundation](https://www.levf.org/). These include but are not limited to * Books * Editorials * Emails * Notes * Published *and* unpublished papers * Results from the [RMR study](https://www.levf.org/projects/robust-mouse-rejuvenation-study-1) The result is an agent which functionally personifies Aubrey de Grey as a digital clone. #### Knowledge Graph The knowledge graph acts a semantic representation of longevity research, powered by the [Longevist](https://www.longevist.xyz/), a VitaDAO curated library spanning over 4000 papers. While reasoning, the agent considers if it needs more information to refine its response. In these cases, it queries the knowledge graph to collect further information, enriching the final output with deeper scientific insights. #### OpenScholar Aubrai's scientific outputs are further refined using a fine-tuned version of [OpenScholar](https://arxiv.org/abs/2411.14199). The model weights used in Aubrai for the OpenScholar retriever and reranker models can be accessed through the Bio Protocol Huggingface [page](https://huggingface.co/bio-protocol/models). # RMR2 ## Project Overview The aim of the RMR project pipeline is an ambitious one: to identify a longevity intervention or treatment program which doubles the remaining lifespan of wild-type adult mice. While the landscape of longevity interventions continues to balloon, nearly all therapies zero in on addressing a single aging hallmark. At LEV Foundation, we believe robust rejuvenation will require targeting multiple aging hallmarks simultaneously, and additionally, that now is the time to begin this approach, a strategy largely underemployed by the research and startup communities. While the RMR program aims to achieve robust rejuvenation in rodents, the implications of a successful outcome reach far beyond laboratory animals. Demonstrable rejuvenation in aged wild-type animals is a key step in securing broad public support of rejuvenation medicine extending beyond ‘soft’ targets such as lifestyle and supplementation, as well as for convincing policymakers. # Study Design ### Objective As in RMR1, the ambition for RMR2 is to achieve "Robust Mouse Rejuvenation". We define this as an intervention or treatment program that: * is applied to mice of a strain with a well-documented mean lifespan of at least 30 months * is initiated at around 12 months younger than the mean lifespan * increases both mean and maximum lifespan by at least 12 months The primary endpoint for the study is to determine the interactions between the various interventions, as revealed by differences between treatment groups (receiving different subsets of the interventions), on overall lifespan. However, we are also investigating aging and morbidity trajectories, causes of death, and functional decline. In this way we will add greatly to the understanding of which benefits these interventions confer and how they synergize, or possibly antagonize. ### Age at study initiation As in RMR1, interventions will begin in mid-late life, between 18-20 months of age, in order to assess the repair/rejuvenation capacity of interventions. The study will run through the remaining lifespan of all mice with the exception of animals selected for cross-sectional analysis at timepoints, as in RMR1. ### Mouse Strain For this second RMR study, we have two well-validated mouse strains to choose from. One option is to use the same pre-aged C57Bl/6J mice as in RMR1. There are a number of practical advantages to using this strain, including that it is the most common strain for biomedical research on mouse lifespan, used in approximately 90% of laboratory studies. As such, naturally aged animals are readily available from Jackson Laboratory (JAX, Bar Harbor, Maine) at a range of advanced ages, permitting studies such as our own, investigating interventions begun in late life. Extensive research has been conducted on C57Bl/6J mice, leading to well- established baseline data for various age-related parameters, which can facilitate comparisons and benchmarking in aging studies. Many interventions of interest to RMR have been developed and tested for efficacy in his strain. However, due to their inbred ancestry and consequent genetic uniformity, C57Bl/6J have disadvantages which are likely relevant for translation of therapies to humans, as they may not exhibit as diverse aging phenotypes as outbred strains, failing to capture the full genetic complexity of aging and age-related diseases seen in human populations, as well as a more limited range of intervention responses. This is a significant tradeoff, and one which remains under careful consideration.Alternatively, we may opt for HET3 mice, which for the first time are now available at scale, pre-aged from JAX. HET3 mice are generated through a four-way intercross (BALB/cByJ × C57Bl/6J F1 females to C3H/HeJ × DBA/2J F1 males), and are the strain utilized by the NIH’s well-established Interventions Testing Program (ITP), which aims to identify and systematically test dietary and drug interventions that can extend healthspan and lifespan in mice with the potential for translation to human aging research. The primary, but significant advantage of conducting aging studies in HET3 mice over inbred strains is because of their increased genetic diversity, which more closely mimics the genetic heterogeneity seen in human populations -- making them a valuable model for studying complex traits and diseases related to aging. HET3 mice also often exhibit slightly longer average lifespans compared to other strains, permitting research to track age-related changes and diseases which develop later in life (although they are somewhat shorter-lived than CL57Bl6/J).While the ITP has been collecting data on HET3 mice for over a decade, some differences in mean and maximum lifespan and intervention responses have been observed across testing sites, and baseline values for parameters like reference blood counts, chemistries, and functional performance are significantly more limited than for C57Bl/6 mice. Additionally, because the HET3 strain is only very recently available pre-aged and at scale, few of the interventions of interest to us have yet been studied in this model. The Study of Longitudinal Aging in Mice (SLAM) conducted by the National Institute on Aging currently aims to assess normative mouse aging and investigate potential differences in aging phenotypes between C57Bl/6J and HET3 mice of both sexes to identify and characterize phenotypic and biological predictors of mouse aging. Results from this study are pending, however, as is phenotypic data on aged HET3 cohorts being collected by JAX labs, so known baselines remain limited. Furthermore, genetically heterogeneous HET3 mice present a challenge when considering interventions such as cell therapies due to immune incompatibility. For these reasons, we expect that as in RMR1, RMR2 will also be conducted in CL57Bl/6J mice. ### Treatment Groups RMR2 is planned to include 10 groups, as in RMR1, including groups receiving just one intervention as to validate that we are successfully recapitulating effects reported in prior work. We continue to reason that very little additional information would result from also including the six possible combinations of two out of four interventions. Three out of four, on the other hand, gives key information, especially on the existence of any antagonistic interactions. ### Controls We again plan to use two types of control for each intervention. Mock treatment controls closely resemble an experimental treatment but lack the active ingredient or activity. They are administered in the same fashion as an active treatment. This might include, for example, a saline injection, giving a gene therapy vector lacking the experimental gene or with the code “scrambled” (nonfunctional), or spiking animal chow with an inactive drug. The other type of control is termed “naïve”, where animals receive only the experimental treatments (if any) assigned to their group, without any additional mock treatments. Comparison between mock and naïve controls allows us to discriminate treatment outcomes from effects which might be related to the act of administration or the vehicle composition. For example in RMR1, animals in the “No mTERT - Naive” group received only rapamycin, HSCs, and a senolytic, while those in the “No mTERT – Mock” group received all three experimental treatments, plus an AAV9 gene therapy vector lacking mTERT. Comparison of outcomes between mock and naïve groups is necessary to distinguish real from placebo effects – in this example, if treatment with the AAV9 vector itself has an effect on the animals, independent of the mTERT gene.Results from the RMR1 study, however, indicate that it is likely not necessary to have equally as many naïve and mock control animals in each group, as little to no effect is observed across groups from administration or vehicle treatment alone. Reducing the size of naïve controls in a given intervention group, for example, would still provide necessary data about possible administration effects, without sacrificing statistical power for in-group analysis. ### Scale of study We aim to conduct RMR2 on a similar scale as RMR1, including 500 male and 500 female mice. In the event of funding limitations, one suboptimal possibility is to conduct RMR2 with only 500 animals to start, which cuts the study size in half, while maintaining statistical power for individual treatment groups. While instead using a single sex would enable us to initiate RMR2 more expediently, it remains a very undesirable option due to significant known sexual dimorphism with respect to both lifespan and intervention effects in rodents and humans alike, which indeed has been observed in RMR1. Other choices for cutting down the number of mice would significantly impact the ability to draw statistically significant conclusions. To elaborate on this: typical “simple” studies in the literature with just two treatment groups rarely use fewer than the 50 mice per treatment group that we are using in RMR1. The many-group, multiplexed nature of our studies affects this in two main ways, which essentially cancel out: on the one hand we can ask about the effect of an intervention across all the five groups that receive it versus those that do not, so effectively the group size for each sex is 250 rather than 50; but on the other hand, the complexity introduces a “multiple hypothesis problem” whereby one expects to see a large difference between SOME pair of groups purely from random chance because there are lots of pairs, meaning that the level of statistical significance required to draw conclusions is higher. Thus, it would be inadvisable to drop below 50 mice per treatment group. We of course get far more from this design of study than the above, not least in terms of synergy information, but that does not change the basic group size requirement just outlined. # Choosing interventions Our primary interest when determining which interventions to include in RMR studies is, of course, the strength of pre-existing evidence pointing to damage reversal. For RMR1 our criteria were extremely stringent: that treatments have already demonstrated lifespan extension individually, and that they did so when begun in mid-late life in wild-type mice. This accomplishes a couple of things. Firstly, any intervention which is capable of extending lifespan in this way must, by definition, be addressing/alleviating all types of damage which cause significant morbidity, through a combination of direct and knock-on effects. The task, then, is to determine if we can extend this further by combining interventions which do this, but through different mechanisms – which introduces a third criterion, namely that the interventions should be highly divergent in their presumed direct targets. For RMR2, our criteria are less stringent, though still focused on damage-reversing therapies. We remain interested in interventions which meet the previous criteria, but now we also consider treatments which may not have clearly established maximum lifespan benefits, but which significantly improve healthspan and/or mean lifespan. In practical terms this differs from RMR1 in that therapies only affecting healthspan are likely to primarily, and robustly, address a single or few drivers of pathology, but don’t appear to have enough systemic knock-on effects to cover all bases and thus increase maximum lifespan. A combination of such treatments, however, might achieve full-spectrum damage repair – perhaps even more so than treatments affecting every system to some more minor degree. ### Duration of benefit The approximate duration of benefit from a single administration of a given intervention is also important to consider. This is especially relevant when selecting more invasive interventions, such as those requiring intravenous or intraperitoneal injection of material. Not only is that process physically and psychologically stressful for animals, it also comes with the risk of complications, particularly when anesthesia is required. Furthermore, invasive treatments which must be given frequently greatly increase the required reagent amounts and technician time required, in addition to being less likely to be therapeutically practical in humans. Therapies which are effective when given infrequently or intermittently are thus greatly preferred when possible. ### Translatability While our combination studies are, in a sense, proof-of-concept for combined intervention effects, we prefer to avoid therapies which are unlikely to have any path to the clinic in the foreseeable future, for example heterochronic parabiosis. This does not preclude the inclusion of intervention variants, however, based on the theme of a promising intervention. We will discuss this further below in the context of saline albumin. ### Technical feasibility and invasiveness There are studies which have yielded impressive results, but which cannot be practically replicated (within a budget that we can consider realistic) at the scale necessary for statistical significance in a multi-intervention animal study. For example: therapeutic plasma exchange or plasma dilution, as previously used, require animals to have surgically implanted cannulae for administration, and typically require a large number of treatments because of the limiting blood volumes which can be exchanged at once. Studies using ‘young plasma’ source plasma directly from sacrificed donor mice, and even those giving only saline-albumin require sacrificed donor mice to supply the red cell component.\ \ Any cell or fluid preparation harvested directly from donors is typically isolated and processed immediately before administration to recipients. Logistically, this can be quite challenging even on a small scale, let alone a study of this size. In the context of HSC transplant from young donors in RMR1, we navigated this challenge by staggering the treatment days and groups from study start, as the study mice were only planned to receive the treatment once. Still, to collect bone marrow for a one-time treatment in 1000 mice, an entire team of technicians had to be brought in from another lab site for 3 separate 5-day spans. Therefore any treatments which we aim to include in RMR2 are considered on the basis of commercial material availability or ease of manufacturing, in conjunction with biological implications of bulk manufacture, for example, stem cell behavior.\ \ Treatments which can be administered in the animal chow have the benefit of permitting continuous, non-invasive dosing and reducing animal handling and stress. For this and other reasons, most studies investigating intervention combinations (or even single interventions), including studies conducted by the NIA’s Intervention’s Testing Program (ITP), are restricted to testing orally-available compounds. Because orally available therapies already receive sufficient attention in lifespan studies, we are largely interested in those treatments which are more difficult to administer, and thus more complex. Unfortunately, any treatment materials which are administered in a way other than orally or topically are considerably more expensive than those which can be consumed, as products must be sterile and GLP manufacturing or similar grade is often necessary or required. But they include essentially all gene and cell therapies, so omitting them amounts to asking for failure.\ \ Additionally, for any therapies which are administered in chow, it must either be acceptable that the amount of a molecule an animal consumes is unknown, or that animals can be singly-housed with rationed feeding. While single animal housing would enable precise dosing of chow-administered treatments, the negative health outcomes linked to social isolation in rodents are undisputed and fail to justify single housing solely for control of food consumption. Investigation of dietary interventions such as caloric restriction can still be, and often are, thus conducted in group-housing conditions through the use of reduced-calorie food rather than controlled consumption volume, which is a decidedly approximate proxy for the real thing. ### Underrepresentation in research As in the above example of orally available molecules being heavily studied by the ITP, we have chosen to focus on therapies with strong evidence, but which are not already extensively covered by the field. This primarily concerns combinations of small molecules such as rapamycin, metformin, resveratrol, NMN, dasatinib + quercetin, fisetin, acarbose, captopril, and similar. In RMR1, our exception was to include a single well-studied intervention, rapamycin, which consistently extends rodent lifespan and thus also serves as a control, allowing us to compare outcomes from RMR with other lifespan extension reports and better gauge any synergies which may emerge from combination therapies. ### Financial feasibility Unfortunately, some very promising interventions would just not be financially justifiable for a study of this scale. For example, in our preparations for RMR1 we received quote approximations for an exciting therapy which would have cost more than $1M to manufacture for 500 mice, just for a single dose. We also carefully consider options for what form an intervention might take, how frequently it would need to be given, how much of a product is needed to achieve therapeutic benefit, and whether the act of repeated dosing is likely to harm the aged animals. Any administration requiring specialized technical skills incurs a labor cost, and thus those which would need to be given weekly or more frequently would significantly increase overall study costs, in addition to material costs. We are cognizant of how a material source can impact the bottom line for cost of a therapy, weighing costs of manufacturing options against potential consequences, such as diminished efficacy or bandwidth restrictions. Additionally, therapies which would require single-animal housing would increase the cost of basics like the number of cages needed, the amount of nesting material, the hours required for cleaning, etc. in the same way that very frequent treatments increase the cost of materials and technician labor. # Top-Line Intervention Choices After several months of evaluating a great many candidates according to the criteria described and explained above, we have tentatively landed on the following choices for RMR2. The first four interventions in this section are primarily considered, while the next four (RMR2+) are additional interventions we would like to include, subject to funding limits. These are of particular interest given the promising results reported in the past 12 months by other groups and their potential to provide critical insight about longevity mechanisms and synergies. As described below, some details remain to be determined, in terms of how the intervention will be constructed or administered. This is ongoing; we will keep our options open until funding is complete, but we are committed to moving as fast as possible in order to hasten the achievement of RMR and thence LEV. **13 Deuterated fatty (arachidonic) acids – D-PUFAs** The first intervention we plan to include in RMR2 consists of deuterated fatty acids, which we have been offered free of charge. Lipid peroxidation occurs as a consequence of metabolism and plays a significant role in cellular dysfunction with aging. Free radicals strip electrons from membrane lipids in a cascading fashion, generating lipid peroxides and other harmful byproducts which damage DNA and proteins. Membrane integrity and fluidity are disrupted, resulting in impaired membrane transport and intracellular signaling, as well as damaging mitochondria, leading to the production of more free radicals. Studies have found that this cascade can be inhibited, however, by replacing reactive hydrogens in candidate fatty acids with deuterium atoms, generating deuterated polyunsaturated fatty acids (D- PUFAs). This isotopic reinforcement makes D-PUFAs resistant to reactive oxygen species (ROS)-initiated chain reactions, allowing them to withstand oxidative damage. Furthermore, it has been demonstrated that the presence of even a small fraction of D-PUFAs among natural PUFAs in membranes will effectively inhibit lipid peroxidation, alleviating disease phenotypes several disease models. Several clinical trials utilizing D-PUFAs have been conducted in humans for a diverse range of pathologies, particularly for cognition and memory, and safety is well-established. Further, D-PUFAs can be provided in animal chow, eliminating unnecessary injections and associated stress on the animals. When consumed, D-PUFAs incorporate into membranes in many tissues, without any reports of toxicity. **Mouse serum albumin - rMSA** Although replicating heterochronic parabiosis or plasma dilution for our study is not feasible, there is promising evidence that monthly administration of virgin albumin in saline is similarly capable of improving multiple healthspan metrics in aging mice and can increase both mean and maximum lifespan. The considerations being weighed in this case are 1) cost of dosing every 3-4 weeks 2) cost of material synthesis and 3) duration of benefit in animals. While constitutive gene therapy-mediated overexpression might technically be possible, it has not, to our knowledge, ever been attempted outside of defect rescue, and it is likely that continuous overproduction of the protein would be detrimental. Any newly-designed construct would need to undergo some relatively time-consuming validation in vivo, though long-term efficacy would still remain unknown, as the system would be incomparable to previous studies. We are currently having early discussions with manufacturers to discuss the costs and timeline of producing physiochemically virgin mouse serum albumin at scale in Pichia pastoris, a yeast expression system which is highly effective for producing pharmaceutical quality heterologous proteins for therapeutics, particularly for proteins which are glycosylated, secreted, and require proper folding. Like any foreign product given to research animals, it must be of high quality and suitable for animal use. Our current estimates for albumin manufacturing are optimistic – currently relying on manufacturers’ ability to inversely scale cost with bulk production. **Mesenchymal stem cells or Exosomes** The progressive loss of stem cell regenerative potential remains one of the most obvious consequences of aging and is a primary focus of rejuvenation therapeutics. Thus, therapies to restore stem cell functionality, including stem cell transplant, are promising strategies for longevity medicine. Stem cell aging remains a high-value target for rejuvenation therapeutics, particularly those aiming for a systemic benefit with possible lifespan extension. Therapeutic administration of stem cells is already demonstrated to improve disease and aging phenotypes in animals and in humans. Our first RMR study (RMR1) also included youthful stem cells as an intervention, however with some key differences, mainly in that it utilized lineage-depleted bone marrow stem cells (HSCs) isolated from young mice. While HSCs populate the cells of the blood and immune system, MSCs constitute an important part of the BM microenvironment that houses HSCs. In addition, the MSC lineage gives rise to many tissues including bone, fat, muscle, and cartilage, as well as endodermal and ectodermal tissues such as neurons, blood vessels, skin, and cells of the liver, pancreas, heart. In this regard, one benefit of MSCs is their relative abundance in the body, as they are enriched in the BM as well as in adipose tissue, skin, muscle, dental pulp, and birth-associated tissues including placenta, umbilical cord, and amniotic fluid and membranes, among other tissues, including peripheral blood. They have been isolated from every mouse tissue and are believed to reside in all postnatal organs. One possibility being studied to enhance MSC benefit is **niche rejuvenation**, which could be coadministered with MSC treatment. One recent study identified NTN1 as a molecule which supports a youthful stem cell environment, and found that donor cells had higher engraftment rates and restorative action in old mice when mice were coadministered supplemental NTN1 We are actively exploring the feasibility of this enhancement, but it is a decision we can make at a late stage. Importantly, of stem cell transplant studies in clinical trials, those which have shown the greatest success utilize **freshly-isolated** cells, as opposed to cryopreserved or culture-expanded. The same is true for HSCs, which is why we opted to increase the project cost by at least $500k (mostly manpower costs; described earlier) in order to avoid freezing. Another option may be to employ “induced MSCs” (iMSCs) derived from iPSCs Since the first report of this approach is very recent (published in 2023), we are still evaluating it. Intravenously administered MSCs have not been shown to integrate into recipient tissues, and rejuvenating effects are generally attributed to secretory factors which may act locally and interact with the immune system. This motivates consideration of ways to increase the half-life of MSCs in the circulation, and we are currently evaluating a potential approach to that. A word should be added here about why we are choosing to administer MSCs rather than the exosomes they generate, which are also indicated to have therapeutic benefit. A number of features argue against exosomes. First, exosomes are very challenging to characterize, and are typically very heterogeneous mixtures. Contents are often unknown, and differ depending on species, age, tissue type, and normal physiology. Thus, obtaining a standardized mixture is particularly challenging. Another drawback to this approach is the durability of benefit. Although it is believed that the vast majority of systemically administered stem cells are eliminated from the system within a few days of injection, there are still significant and much longer-lasting physiological changes which result from body’s response to cell injections, which are not expected to occur with exosome treatment. It seems likely that the benefits of MSC therapy are via the ability of transplanted cells to induce changes in resident cells, promoting the switch to a regenerative phenotype, which further rejuvenates cells and tissues downstream. Some of these induced changes are not expected to occur without the cells themselves, thereby limiting the extent of tissue rejuvenation which can be achieved with exosomes alone. **Partial cellular reprogramming** Partial reprogramming has attracted substantial interest in recent years both from a research and investment standpoint due to its potential for rejuvenation extending beyond individual cells to affect entire tissues and organ systems. The process begins with rapid metabolic changes, as cells shift toward more youthful energy utilization patterns. This metabolic remodeling is crucial, as it provides the necessary substrates and energy for subsequent rejuvenation processes while simultaneously influencing epigenetic modifications through metabolite availability. As these initial metabolic changes take hold, they trigger widespread epigenetic remodeling. Key metabolites like NAD+ and α-ketoglutarate serve as essential cofactors for epigenetic enzymes, enabling the restoration of youthful DNA methylation patterns and histone modifications. This epigenetic rejuvenation then feeds back to enhance metabolic function by modulating the expression of metabolic genes, creating a self-reinforcing loop. Simultaneously, improved energy availability and epigenetic remodeling together enhance cellular protein quality control systems, leading to better clearance of damaged proteins and improved cellular function. The coordination between these fundamental processes - metabolism, epigenetics, and proteostasis - creates a robust foundation for tissue-specific rejuvenation. In muscle tissue, for example, these changes manifest as improved contractile function and better energy utilization. In neurons, they support enhanced synaptic plasticity and neurotransmission. Hepatocytes show improved metabolic and detoxification capabilities. These tissue-specific improvements, in turn, contribute to systemic benefits through enhanced organ function and improved inter-tissue communication. The systemic nature of rejuvenation is further amplified by the interconnected stress response pathways that are activated during partial reprogramming. These pathways, including the heat shock response, unfolded protein response, and DNA damage response, work together to enhance cellular resilience across tissues. Key regulatory hubs like mTOR, sirtuins, and FOXO factors integrate these various processes, ensuring coordinated responses throughout the organism. This molecular orchestra creates a comprehensive rejuvenation program that can restore youthful function at multiple biological scales - from individual cells to entire organ systems. The most responsive cell types to partial reprogramming tend to be those with high metabolic activity and critical regulatory functions, creating cascading benefits throughout the organism. Skeletal muscle cells, for instance, show particularly robust responses, with enhanced mitochondrial function, improved force generation, and better metabolic regulation. This muscle rejuvenation extends beyond mere physical strength - it influences whole-body metabolism through improved glucose handling and myokine secretion, potentially affecting systemic aging processes. Neurons represent another highly responsive cell type, with partial reprogramming enhancing their plasticity, metabolic efficiency, and synaptic maintenance. The rejuvenation of neuronal populations, particularly in regions like the hippocampus and hypothalamus, may have far-reaching effects on longevity through improved cognitive function and better neuroendocrine regulation. The hypothalamic-mediated changes can affect everything from energy metabolism to immune function, creating organism-wide benefits. The liver's high responsiveness to partial reprogramming is particularly significant for longevity. Rejuvenated hepatocytes show enhanced metabolic flexibility, improved protein synthesis, and better toxin clearance. These improvements affect the entire organism through better regulation of blood glucose, more efficient protein homeostasis, and enhanced detoxification capacity. The liver's central role in metabolic regulation means these improvements can significantly impact overall health span. Stem cell populations across various tissues also show marked improvements with partial reprogramming. Enhanced stem cell function in bone marrow, muscle, and other tissues improves tissue maintenance and repair capacity. This improved regenerative potential could help maintain organ function with age, potentially extending both lifespan and healthspan. The rejuvenation of stem cell niches may be particularly important, as these microenvironments influence stem cell behavior and tissue homeostasis. Achieving efficient and safe delivery of reprogramming factors to specific cells or tissues in vivo, however, still presents a considerable challenge and the development of practical, targeted, and cost-effective delivery methods is vital for successful application. The delivery of these factors has historically been achieved using viral vectors or genetic modifications, however recent innovations have focused on liposome-mediated delivery as mRNA, and even chemical induction of reprogramming factors using reagents and small molecules. **Anti-IL-11** The pro-inflammatory cytokine IL-11 is increasingly recognized as a significant component of the senescence-associated secretory phenotype (SASP) and has emerged as a promising longevity target due to its central role in age-related fibrosis and inflammation across multiple tissues. IL-11 production is upregulated in response to oxidative stress as a compensatory mechanism, yet sustained IL-11 activity paradoxically worsens tissue damage by promoting reactive oxygen species (ROS) production. This accumulation of ROS leads to cellular senescence, a condition where cells lose the ability to divide and repair tissue effectively. In the liver, for example, increased IL-11 exacerbates oxidative stress, aggravating liver fibrosis and reducing regenerative capacity (Nishina et al., 2012). In mice, genetic deletion or pharmacological inhibition of IL-11 signaling has recently demonstrated remarkable therapeutic effects in key organs that typically deteriorate with age. In the heart, IL-11 inhibition prevents and reverses cardiac fibrosis by blocking myofibroblast activation and reducing extracellular matrix deposition, ultimately preserving cardiac function. Similarly, in the liver, disrupting IL-11 signaling reduces hepatic stellate cell activation and fibrosis, while improving metabolic parameters and glucose homeostasis. These effects appear to be mediated through the interruption of ERK/MAPK and STAT3 signaling pathways, which are key drivers of cellular senescence and tissue dysfunction. (Schafer et al., 2017; Chen et al., 2020). The therapeutic potential extends beyond individual organs, as IL-11 inhibition shows systemic benefits through its effects on stromal cells and the broader inflammatory environment. For example, increased IL-11 with age dysregulates immune responses by stimulating persistent inflammation, which causes immune cells to infiltrate tissues. This inflammatory environment damages tissues and alters the normal healing process, resulting in a pro-fibrotic state rather than resolution. In cardiovascular tissue, for instance, this persistent inflammation underpins the development of age-related heart failure and other cardiovascular diseases (Xu et al., 2002). In adipose tissue, reduced IL-11 signaling decreases inflammation and improves metabolic health, while in skeletal muscle, it may help maintain tissue integrity during aging. Human studies have revealed increased IL-11 expression in various age-related pathologies, including heart failure, liver cirrhosis, and chronic inflammatory conditions, suggesting strong translational relevance. The broad tissue distribution of IL-11 and its signaling components, combined with its role in fundamental aging processes like fibrosis and inflammation, positions IL-11 inhibition as a potentially powerful intervention for extending healthspan. Research in aged animal models indicates that IL-11 inhibition not only improves tissue- specific functions but may also contribute to lifespan extension. By addressing chronic inflammation, reducing fibrotic progression, and improving overall tissue health, IL-11 blockers have shown promise in increasing healthspan and potentially extending lifespan (Widjaja et al., 2024). The fact that mice lacking IL-11 signaling show improved health outcomes across multiple organ systems suggests that targeting this pathway could offer comprehensive protection against age-related decline. **CDC42 inhibition – CASIN** Elevation of Cdc42, a small RhoGTPase, plays a significant role in the aging process by disrupting cellular functions essential for maintaining tissue homeostasis. As individuals age, Cdc42 activity naturally increases in various cell types, including hematopoietic stem cells (HSCs), mesenchymal stem cells, and intestinal epithelial cells. This elevation contributes to functional declines in cell populations critical for regeneration and repair. For instance, in HSCs, increased Cdc42 levels lead to decreased regenerative capacity and cellular exhaustion, which weakens the immune system’s ability to respond to pathogens and is a core contributor to immunosenescence in older adults (Geiger et al., 2007; Florian et al., 2020, Wiley). The causation of Cdc42 elevation in aging is associated with intrinsic cellular signals and age-related changes in the cellular microenvironment. Factors like oxidative stress, altered lipid composition in cell membranes, and shifts in the cytokine milieu with age contribute to amplifying Cdc42 activity. For example, the chronic inflammatory state of aging, known as “inflammaging,” promotes increased Cdc42 activity, leading to the production of pro-inflammatory cytokines and accelerating tissue degeneration (Ito et al., 2014, PLOS One; Wang et al., 2007, PNAS). Such effects can disrupt insulin and leptin signaling, exacerbating age-related metabolic disorders such as obesity and type 2 diabetes (Umbayev et al., 2023, MDPI). The pathophysiological implications of elevated Cdc42 extend across various systems. In tissues dependent on precise cellular architecture, like neural and epithelial systems, Cdc42-induced disruptions in cell polarity can lead to structural disorganization and functional decline. Elevated Cdc42 levels accelerate aging in HSCs, impairing blood formation and immune responses, while also contributing to chronic inflammation that further degrades tissues like the skin and bone marrow (Geiger et al., 2007, Taylor & Francis; Nalapareddy et al., 2021, Cell). These findings underscore Cdc42 as a key player in degenerative diseases linked to aging, making it a prime therapeutic target for age-related pathologies. Thus, inhibiting Cdc42 activity offers potential benefits, especially with compounds like CASIN, a small molecule inhibitor. CASIN has shown promise in preclinical studies by reducing Cdc42 activity, which has restored functionality in aged HSCs, enhanced their regenerative capacity, and decreased systemic inflammation (Florian et al., 2012, Cell Stem Cell). Such inhibition not only reduces senescence markers but also addresses inflammaging at its cellular root, offering a strategy to potentially extend healthy lifespan by preserving tissue function, improving immune responses, and reducing age-related degenerative processes. CASIN and other Cdc42 inhibitors thus highlight a promising approach to rejuvenating stem cell populations and addressing aging’s systemic impacts at the molecular level (Florian et al., 2020, Wiley). **Senolysis (Rockfish)** The potential senolytic mechanism of long chain fatty acid CoA ligase inhibition is rooted in the distinct metabolic vulnerabilities of senescent cells. These cells demonstrate markedly elevated levels of lysophosphatidylcholine and free arachidonic acid, similar to the lipid profile seen in ferroptotic cells - a connection particularly relevant given recent evidence that senescent cells show increased sensitivity to ferroptosis inducers. The accumulation of these bioactive lipids suggests compromised membrane homeostasis, which has been demonstrated to correlate with increased sensitivity to additional membrane stress in multiple models of cellular senescence. By inhibiting long chain fatty acid CoA ligase, we would prevent the activation of free fatty acids to their CoA derivatives, blocking their incorporation into phospholipids and their entry into beta-oxidation. This would be particularly devastating for senescent cells, which already show impaired lipid homeostasis and increased membrane permeability. The mechanism is analogous to the demonstrated senolytic activity of dasatinib, which disrupts membrane integrity, but potentially more selective due to the pre- existing lipid abnormalities in senescent cells. Supporting this approach, recent studies have shown that senescent cells exhibit reduced expression of membrane repair proteins and decreased capacity to handle acute membrane stress. The combinatorial effect of existing lysoPC-mediated membrane disruption, elevated free AA levels, and blocked fatty acid metabolism would likely exceed the survival threshold specifically in senescent cells, while normal cells could maintain viability through intact compensatory mechanisms and baseline membrane stability. **Oxytocin Therapy** Oxytocin therapy has emerged as a promising intervention for extending lifespan and promoting rejuvenation in various animal models, with studies consistently highlighting its capacity to reverse age- related decline and restore function across multiple systems, including the muscular, hepatic, skeletal, and nervous systems. **Lifespan Extension**: In aged mice, oxytocin treatment has been linked to increased healthspan and lifespan through systemic rejuvenation mechanisms. Research by Díaz-del Cerro et al. (2022) demonstrated that oxytocin improves homeostatic regulation and reduces inflammation, key factors in extending healthspan. Mice treated with oxytocin exhibited improved metabolic health and resilience, delaying the onset of age-related conditions (Díaz-del Cerro et al., 2022). **Muscle Regeneration:** Oxytocin enhances the regenerative capacity of aged muscle by activating muscle satellite cells. Erdman (2021) showed that systemic administration of oxytocin in aged mice restored muscle repair to youthful levels, mediated by the activation of the MAPK/ERK pathway. This pathway promotes the proliferation and differentiation of muscle progenitor cells, enabling efficient tissue repair and reducing muscle atrophy (Erdman, 2021). **Hepatic and Bone Rejuvenation**: Oxytocin therapy has also shown promise in restoring liver and bone health. Zhai et al. (2021) found that oxytocin promotes liver regeneration by increasing hepatocyte proliferation via STAT3 signaling. Similarly, Fernandes-Breitenbach et al. (2022) observed improvements in bone density and strength in aging rats treated with oxytocin. The hormone stimulated osteoblast activity and reduced bone resorption, thereby reversing age-related osteoporosis (Zhai et al., 2021; Fernandes-Breitenbach et al., 2022).
**Cognitive and Neuroprotective Benefits** Oxytocin has been shown to enhance brain function and protect against neurodegeneration in aged rodents. Studies by Carter and Kingsbury (2022) demonstrated that oxytocin increases neurogenesis and synaptic plasticity while reducing neuroinflammation. These effects, mediated through the upregulation of brain-derived neurotrophic factor (BDNF), suggest that oxytocin supports cognitive health during aging (Carter & Kingsbury, 2022). * Molecular mechanisms underpinning oxytocin’s rejuvenative effects include activation of MAPK/ERK and STAT3 signaling pathways, reduction of oxidative stress, and modulation of inflammatory cytokines. Typical therapeutic regimens involve subcutaneous or intraperitoneal administration at doses of 0.5–2 mg/kg/day over periods ranging from days to weeks, depending on the target system. #### **Potential Interactions** D-PUFAs + rapamycin o D-AA protects membranes while mTOR inhibition enhances autophagy Potential synergies: * Enhanced mitochondrial quality control * Improved protein homeostasis * Better cellular recycling * Reduced inflammatory signaling **D-PUFAs + senolysis by arachidonic acid buildup** Deuteration slows AA metabolism, in turn retarding the generation of pro-inflammatory eicosanoids while maintaining membrane structural properties and signaling functions. In combination with an AA- mediated senolytic, cellular responses become quite complex and challenging to predict. The simultaneous administration of d-AA and blockade of long chain fatty acid CoA ligase may create a unique metabolic situation where neither regular AA nor d-AA can be effectively activated to their CoA forms, leading to accumulation of unesterified fatty acids, potentially disrupting membrane organization and cellular signaling pathways. While the deuteration still protects against oxidative metabolism where it occurs, many of the beneficial effects of d-AA might be compromised due to the inability to properly incorporate it into cellular lipids. This combination therefore presents a biochemical paradox where the protective effects of d-AA could be overshadowed by the cellular stress of accumulated free fatty acids and disrupted lipid homeostasis. These effects, however, could very well be dose-dependent, as senescent cells are predicted to be uniquely vulnerable to CoA ligase blockade, sparing healthy cells and tissues at low doses, thus opening the possibility that the combination of interventions potentiates the rejuvenation effects of both. The only way to determine if outcomes are synergistic or antagonistic is to combine the interventions and testing dose responses. **Reprogramming + rMSA** One possible reason for the systemic rejuvenation possible with partial reprogramming is due to its ability to restore normal gene expression patterns for critical pathways which become disrupted with age. For example, changes to serum albumin synthesis, structure, and function are well-documented in aging, with transcriptional changes attributed to altered promoter methylation in hepatic cells. Similarly, methylation changes are one reason for global reduction in the expression and activity of antioxidant enzymes in aging, which, in combination with the reduced capacity of albumin, results in doubly diminished cellular protection against free radicals. Because oxidative stresses accumulate so readily with age causing damage to numerous cellular structures, therapeutic combinations increasing antioxidant capacity through different mechanisms may yield significant synergistic benefits. This includes other interventions currently in consideration, such as D-PUFAs to reduce lipid peroxidation, senolysis to eliminate malfunctioning cells generating increased ROS, IL-11 inhibition to counteract fibrosis and restore normal tissue function, which in turn, lowers the production of pro- inflammatory factors and ROS production, etc. ### “Baseline” treatments Combination therapies are only valuable if their benefit exceeds that of the best known alternative. To date, the most effective rejuvenation treatments are rapamycin, caloric restriction, and exercise. We carefully considered these in the context of RMR1, opting to include rapamycin as one of the four interventions for comparison. For RMR2, we are considering giving rapamycin to ALL the animals, i.e. as a baseline intervention without untreated controls. This would allow us to gauge the efficacy of other rejuvenation interventions when the overall damage burden is already slightly lowered. Similarly, we have determined that animals in the RMR2 study will have access to a running wheel in their cages, permitting voluntary exercise. While the animals in RMR1 are provided some enrichment such as nesting material, wheels are not standard in conventional rodent housing. Physical activity is known to be a strong determinant of healthspan in both animals and humans, and we believe that no intervention can be maximally effective in obese, inactive mice. We do not consider this addition to be an “intervention” in itself, but rather a basic requirement in order to delay aging pathologies. # $AUBRAI The distribution plan for the total supply of 2,000,000 $AUBRAI tokens is allocated among different stakeholders within the community. Here's a breakdown of the allocation:
1. Launchpad: 20% (400,000 tokens) will be sold to the public. 2. Liquidity Pool: 6% (120,000 tokens) are set aside for the liquidity pool. 3. Treasury: 15% (300,000 tokens) is dedicated to the ecosystem treasury. This allocation is earmarked for community incentives and strategic initiatives. This will sit in a DAO-controlled multi-sig wallet. 4. Initial Funders: 20.1% (402,000 tokens) is reserved for initial funders of the RMR2 study. Half of this allocation is subject to a 4-year vesting schedule and the other half is immediately liquid upon launch. 5. LEVF: 10% (200,000 tokens) are set aside for the Longevity Escape Velocity Foundation (LEVF). This allocation is subject to a 4 year vesting schedule with a 1 year cliff. 6. VitaDAO: 22% (440,000 tokens) are set aside for VitaDAO as the core initiators of the Aubrai project. Half of this allocation is subject to a 4-year vesting schedule and the other half is immediately liquid upon launch. 7. BIO: 6.9% (138,000 tokens) are set aside for BIO as co-initiators of the Aubrai project. This allocation is fully liquid upon launch. # Tokenomics The distribution plan for the total supply of 2,000,000 $AUBRAI tokens is allocated among different stakeholders within the community. Here's a breakdown of the allocation:
1. Launchpad: 20% (400,000 tokens) will be sold to the public. 2. Liquidity Pool: 6% (120,000 tokens) are set aside for the liquidity pool. 3. Treasury: 15% (300,000 tokens) is dedicated to the ecosystem treasury. This allocation is earmarked for community incentives and strategic initiatives. This will sit in a DAO-controlled multi-sig wallet. 4. Initial Funders: 20.1% (402,000 tokens) is reserved for initial funders of the RMR2 study. Half of this allocation is subject to a 4-year vesting schedule and the other half is immediately liquid upon launch. 5. LEVF: 10% (200,000 tokens) are set aside for the Longevity Escape Velocity Foundation (LEVF). This allocation is subject to a 4 year vesting schedule with a 1 year cliff. 6. VitaDAO: 22% (440,000 tokens) are set aside for VitaDAO as the core initiators of the Aubrai project. Half of this allocation is subject to a 4-year vesting schedule and the other half is immediately liquid upon launch. 7. BIO: 6.9% (138,000 tokens) are set aside for BIO as co-initiators of the Aubrai project. This allocation is fully liquid upon launch. ### Addresses * [$AUBRAI](https://basescan.org/token/0x9d56c29e820Dd13b0580B185d0e0Dc301d27581d) * [Vesting Contract](https://basescan.org/address/0xb08f663DcCE6028F7197f4718157AB3b34c373cb) * [VitaDAO](https://app.safe.global/home?safe=base:0x84cfF3C47eC2DA624834436C589E0fBdC73B219d) * [BIO](https://app.safe.global/home?safe=base:0xd9C6Ee1547Fd6d48F8872dD866473893Bbe8A1Ab) * [Treasury](https://app.safe.global/home?safe=base:0x44dC2dceaA22c7EF6B2E2cF2362Fd3FB476b7c2C) * LEVF (comming soon) :information\_source: Distributions will be finalized shortly # Legal Info ### Crypto-Asset Type and Functionality: Utility Token (DAO Governance). Functionality available at the time of issuance.
### Purchaser rights and obligations: Proposing and Voting on DAO governance proposals.
### Representations: The Participant is capable of fully evaluating the merits and risks of purchasing the Tokens. The Participant is fully able to bear the risks associated with the Token Sale and agrees to bear such risks. Furthermore, the Participant has sufficient technical understanding of cryptographic tokens, network protocols, smart contracts, token storage mechanisms, and distributed networks or distributed ledger technology in general to understand the terms of this Token Sale, and to appreciate the risks and implications of entering into this Token Sale. THE PARTICIPANT UNDERSTANDS AND EXPRESSLY ACCEPTS THAT THE TOKENS WILL BE CREATED AND DELIVERED TO THE PARTICIPANT AT THE SOLE RISK OF THE PARTICIPANT ON AN “AS IS,” “UNDER DEVELOPMENT” AND “AS AVAILABLE” BASIS, WITHOUT WARRANTIES OF ANY KIND. The Participant understands and expressly accepts that the Participant has not relied on any representations or warranties made by VitAubrAI outside of this Token Sale , including, but not limited to, conversations of any kind, whether through oral or electronic communication (including any communications on social media, which includes, but is not limited to Telegram, Discord, WhatsApp, and X), or any white paper, offering memorandum, or other document. WITHOUT LIMITING THE GENERALITY OF THE FOREGOING, THE PARTICIPANT ASSUMES ALL RISK AND LIABILITY FOR THE RESULTS OBTAINED BY THE USE OF ANY TOKENS AND REGARDLESS OF ANY ORAL OR WRITTEN STATEMENTS MADE BY VITAUBRAI, BY WAY OF TECHNICAL ADVICE OR OTHERWISE, RELATED TO THE USE OF THE TOKENS. THE PARTICIPANT ACKNOWLEDGES THAT THE INFORMATION INCLUDED IN THIS TOKEN SALE CONSTITUTE SUFFICIENT INFORMATION FOR THE PARTICIPANT TO MAKE AN INFORMED PURCHASE DECISION. THE PARTICIPANT ACKNOWLEDGES THAT IT HAS BEEN ADVISED TO CONSULT WITH, AND HAS CONSULTED WITH, THE PARTICIPANT’S OWN ATTORNEY, ACCOUNTANT, TAX ADVISOR, AND INVESTMENT ADVISOR WITH RESPECT TO THE PURCHASE OF THIS TOKEN SALE AND THE TOKENS. ANY SPECIFIC ACKNOWLEDGMENT WITH RESPECT TO ANY STATEMENT CONTAINED IN THIS SECTION SHALL NOT BE DEEMED TO LIMIT THE GENERALITY OF THIS REPRESENTATION AND WARRANTY. The Participant understands that Participant has no right against VitAubrAI or any other Person except in the event of VitAubrAI’s breach of this Token Sale, gross negligence or intentional fraud. VitAubrAI’S AGGREGATE LIABILITY ARISING OUT OF OR RELATED TO THIS TOKEN SALE, WHETHER ARISING OUT OF OR RELATED TO BREACH OF CONTRACT, TORT OR OTHERWISE, SHALL NOT EXCEED THE TOTAL OF THE PURCHASE AMOUNT. NEITHER VITAUBRAI NOR ITS REPRESENTATIVES SHALL BE LIABLE FOR CONSEQUENTIAL, INDIRECT, INCIDENTAL, SPECIAL, EXEMPLARY, PUNITIVE OR ENHANCED DAMAGES, LOST PROFITS OR REVENUES OR DIMINUTION IN VALUE, ARISING OUT OF OR RELATING TO ANY BREACH OF THIS TOKEN SALE. The Participant understands that Participant bears sole responsibility for any taxes as a result of the matters and transactions contemplated by this Token Sale , and any future acquisition, ownership, use, sale or other disposition of Tokens by the Participant. This includes the tax implications associated with any determination (including those by VitAubrAI or any tax authority) that this Token Sale or any Token represents a security, a right to a security, an asset or commodity, a right to an asset or commodity, a utility or use right, or other non-security Token Sale. To the extent permitted by Law, the Participant agrees to indemnify, defend and hold VitAubrAI or any of its affiliates, directors, officers, employees or agents (including developers, auditors, contractors or founders) harmless for any claim, liability, assessment or penalty with respect to any taxes (other than any net income taxes of VitAubrAI that result from the issuance of Tokens to the Participant, or associated with or arising from the Participant’s purchase of Tokens hereunder, or the use or ownership of Tokens. ### Specific Risk Representations: #### 1. Risks Associated with the Issuer of the Crypto-Assets The financial stability and operational continuity of the issuer are essential to the success of the project. Potential risks include: * **Financial Risk**: The issuer may not generate sufficient revenue or funding to sustain operations, leading to reduced capacity to support the project. * **Governance Risk**: Key decisions depend on the issuer’s management team. Mismanagement, internal conflicts, or lack of expertise could negatively affect the project. * **Legal and Regulatory Risk**: Changes in applicable laws or enforcement actions against the issuer may restrict or prevent the issuer from carrying out its activities. * **Reputation Risk**: Negative publicity, market perception, or loss of trust in the issuer could undermine adoption and Token value. #### 2. Risks Associated with the Offer and/or Admission to Trading The process of offering or listing the Token carries specific risks: * **Offer Execution Risk**: Technical or administrative errors during the Token sale may lead to failed transactions, loss of funds, or allocation disputes. * **Market Access Risk**: Admission to trading is not guaranteed and depends on trading venue decisions and compliance with their listing requirements. * **Liquidity Risk**: Even if admitted to trading, there is no guarantee of active secondary markets. Tokenholders may be unable to sell their Tokens at desired prices or within a reasonable timeframe. * **Regulatory Risk**: National competent authorities may impose restrictions on the offer or trading of the Token, including suspension or delisting. #### 3. Risks Associated with the Crypto-Assets The Token itself has inherent risks that may impact holders: * **Utility Limitation Risk**: The Token’s utility may not materialize as planned, or the features may be delayed, reduced, or limited in scope. * **Valuation Risk**: As a utility Token, the Token does not represent ownership or profit rights. Its value may fluctuate significantly based solely on supply, demand, and perceived utility. * **Concentration Risk**: If large allocations are held by a small number of holders, they may exert disproportionate influence on Token price and circulation. * **Transferability Risk**: Technical or regulatory restrictions could limit the ability to transfer or exchange Tokens. #### 4. Risks Associated with Project Implementation Execution of the project roadmap depends on internal and external factors: * **Development Risk**: The project may face delays in development, scaling, or delivery of promised functionalities. * **Dependency Risk**: The project may depend on third-party service providers (e.g., infrastructure, cloud hosting, custodians) whose failure could impact project operations. * **Funding Risk**: The proceeds from the Token offer may not be sufficient to achieve stated milestones, leading to scope reductions or abandonment of certain features. * **Operational Risk**: Inadequate internal processes, staffing shortages, or misallocation of resources could negatively affect project outcomes.
**5. Risks Associated with the Technology Used and Mitigation Measures** The underlying blockchain and related technologies carry inherent risks: * **Smart Contract Risk**: Vulnerabilities in Token or protocol smart contracts could be exploited, resulting in financial loss or disruption of services. * **Mitigation**: Contracts are subject to third-party security audits prior to deployment. * **Blockchain Risk**: The Token depends on the stability and security of the underlying blockchain. Network failures, forks, or consensus attacks could impact Token functionality. Mitigation: The project uses a widely adopted blockchain with a strong validator community. * **Cybersecurity Risk**: Unauthorized access, hacks, or phishing attacks could compromise wallets, user data, or project infrastructure. * **Mitigation**: Multi-signature wallets, penetration testing, and ongoing monitoring are implemented. * **Scalability and Performance Risk**: High transaction volumes may cause congestion or higher fees, reducing usability.Future upgrades and integration with scaling solutions are being explored. # Helpful Links Here you can find a collection of helpful links to our community channels, social media pages, and other important resources. **Socials** * ​[**X**](https://x.com/AUBRAI_)**:** Follow Aubrai on X for the latest news, updates, and agent highlights. * ​[**Discord**](https://discord.com/invite/3S3ftnmZYD)**:** Join our Discord server to connect with the team, developers, and other community members. **Ecosystem & Governance** * ​[**AUBRAI Token**](https://app.gitbook.com/o/NCQ5aGXwXZkRrGHN7L6a/s/8prnQMolUTygNUGfhG4b/)**:** Learn more about the `$AUBRAI` token. * [**AUBRAI Governance**](https://common.xyz/aubrai/): Use `$AUBRAI` to govern the future of the Aubrai agent. * [**AUBRAI Treasury**](https://app.safe.global/transactions/queue?safe=base:0x44dC2dceaA22c7EF6B2E2cF2362Fd3FB476b7c2C): Keep track of assets held by the Aubrai agent.