Discovery Pipeline

Aberrant activation of Janus kinase (JAK) and protein kinase B (AKT) signaling pathways is a hallmark of multiple cancer types, driving uncontrolled proliferation, survival, and resistance to therapy. The JAK-STAT pathway is crucial for cytokine signaling and immune regulation, while the AKT pathway, a key component of PI3K signaling, promotes cell growth, metabolism, and survival. Dysregulation of both pathways is frequently observed in hematological malignancies, solid tumors, and treatment-resistant cancers. Simultaneous inhibition of JAK and AKT may be a highly promising therapeutic strategy. Targeting these two pathways together offers a good approach to suppress tumor progression, enhance apoptosis, and overcome drug resistance.

JAK and AKT inhibitors have individually demonstrated clinical efficacy in cancers such as leukemia, lymphoma, breast, lung, and prostate cancer. However, monotherapies often fail due to compensatory activation between these pathways, leading to resistance and limited therapeutic durability. Dual inhibition of JAK and AKT provides a more comprehensive blockade of oncogenic signaling, preventing cross-talk-driven resistance mechanisms. Developing a small-molecule dual inhibitor with optimized selectivity and pharmacokinetics could revolutionize targeted therapy for JAK- and AKT-driven malignancies, offer a more durable and effective cancer treatment.

We are currently developing a dual inhibitor that inhibit JAK/STAT and PI3K/AKT pathway with enhanced potency, selectivity, and metabolic stability. Using AI-driven molecular screening and structure-based drug design, we have successfully generated small molecules that demonstrate good binding affinity to JAK and AKT, as confirmed by in-vitro radioactive kinase assays. Our pipeline compounds has shown inhibition of AKT and JAK enzymes positioning it as a promising candidate for further pre-clinical assessment. Ongoing primary ADME and safety studies marking a critical step toward a development of novel, dual-targeted therapy for multiple aggressive cancers.

Non-melanoma skin cancer (NMSC) is among the most prevalent malignancies, primarily driven by chronic ultraviolet (UV) radiation exposure, leading to DNA damage and genetic alterations. While many cases are treatable, mutations in key oncogenes, particularly BRAF, have emerged as critical drivers of uncontrolled cellular proliferation in subsets of NMSC. The BRAF gene encodes a serine-threonine kinase that plays a pivotal role in the mitogen-activated protein kinase (MAPK) signaling pathway, a crucial regulator of cell growth and survival. Aberrant activation of this pathway due to BRAF mutations, such as V600E, results in unchecked cell division and tumor progression, highlighting BRAF as a promising therapeutic target in skin cancer treatment. Targeted BRAF inhibitors have revolutionized melanoma therapy, demonstrating selective inhibition of mutant BRAF kinase activity, effectively suppressing MAPK signaling and halting cancer cell proliferation.

We are currently focusing on developing small-molecule BRAF inhibitors with next-generation specificity and optimized drug-like properties. Using AI-driven molecular design and in-silico screening, we have successfully identified and evaluated potent hit molecules with promising BRAF inhibition profiles. By integrating computational drug discovery, structural optimization, and experimental validation, our goal is to deliver a next-generation BRAF inhibitor that can effectively target NMSC, overcome resistance mechanisms, and advance toward clinical development.

Squamous cell carcinoma (SCC) is a highly aggressive form of non-melanoma skin cancer (NMSC), often associated with genetic alterations in key signaling pathways that drive tumor growth and progression. Among these, the fibroblast growth factor receptor (FGFR) family, which regulates cell proliferation, differentiation, and angiogenesis, has emerged as a critical therapeutic target. Aberrant FGFR signaling, caused by FGFR gene amplification, mutations, or ligand overexpression, leads to unchecked tumor cell proliferation and survival in SCC. Given its role in tumor progression, FGFR inhibition represents a promising therapeutic approach to suppress oncogenic signaling and halt SCC growth.

Targeting FGFR in SCC has gained significant attention, with FGFR inhibitors showing promise in preclinical and clinical settings. Small-molecule FGFR inhibitors, have demonstrated efficacy in FGFR-driven cancers by selectively inhibiting FGFR kinase activity and disrupting downstream signaling through the MAPK and PI3K pathways. In SCC, FGFR inhibition has been shown to induce tumor cell apoptosis, impair angiogenesis, and enhance sensitivity to existing treatments, making it a viable therapeutic strategy. Given the heterogeneous nature of SCC, combining FGFR inhibitors with immune checkpoint blockade or chemotherapy may further improve therapeutic outcomes.

We are in the initial phase of developing small-molecule FGFR inhibitors with optimized selectivity and potency against FGFR-driven SCC. Using AI-driven molecular design and in-silico screening, we have identified high-affinity FGFR inhibitors with good kinase selectivity. By integrating computational drug discovery, structural optimization, and functional validation, we aim to advance next-generation FGFR inhibitors that can effectively target SCC, improve patient outcomes, and contribute to the expanding landscape of precision oncology.

Hypertension remains a leading risk factor for cardiovascular disease, stroke, and organ damage, driven by vascular dysfunction and increased vascular resistance. One of the key regulators of vascular tone and smooth muscle contraction is the Rho-associated coiled-coil kinase (ROCK) pathway, which plays a crucial role in vascular remodeling, endothelial dysfunction, and arterial stiffness. Among its isoforms, ROCK2 is predominantly expressed in vascular smooth muscle cells and the heart, making it an attractive therapeutic target for hypertension and related cardiovascular disorders. Inhibition of ROCK2 has been shown to induce vasodilation, improve endothelial function, and reduce pathological vascular remodeling, highlighting its potential as an effective antihypertensive strategy.

ROCK inhibitors have demonstrated vasodilatory and cardioprotective effects, but their non-selective inhibition of both ROCK1 and ROCK2 has been associated with dose-limiting side effects. The development of ROCK2-selective inhibitors offers a safer and more targeted approach to reducing blood pressure while minimizing off-target effects. Selective ROCK2 inhibition not only lowers vascular resistance but also has broader therapeutic potential, including reducing fibrosis, inflammation, and oxidative stress in cardiovascular tissues. Given these advantages, highly selective ROCK2 inhibitors could redefine hypertension treatment, offering a novel and more refined approach to vascular protection.

We are currently focusing on developing a selective small-molecule ROCK2 inhibitor, designed to precisely target vascular dysfunction without affecting ROCK1-related pathways. Using AI-driven molecular docking and in-silico screening, we have identified a potent ROCK2-selective inhibitor with good binding affinity, demonstrating robust kinase inhibition and promising pharmacokinetic properties. Our identified compound has shown high selectivity for ROCK2 over ROCK1, ensuring targeted therapeutic action and expected reduced potential adverse effects. With good receptor binding, our ROCK2 inhibitor is now ready to advance through further preclinical investigation, marking a significant step toward a next-generation antihypertensive therapy that could provide improved vascular health, lower blood pressure, and enhanced cardiovascular protection.

Diabetes is a major metabolic disorder that significantly increases the risk of cardiovascular and renal complications, collectively known as cardiorenal and metabolic syndrome (CVRM). One of the most promising therapeutic targets in diabetes management is sodium-glucose co-transporter 2 (SGLT2), which plays a crucial role in renal glucose reabsorption. Under diabetic conditions, SGLT2 is overexpressed in the kidneys, leading to excessive glucose reabsorption, hyperglycemia, and increased renal stress. Inhibiting SGLT2 promotes glucose excretion through urine, thereby lowering blood sugar levels and reducing the metabolic burden on the kidneys and cardiovascular system. Given its dual glycemic and organ-protective benefits, SGLT2 inhibition has emerged as a transformative approach in diabetes therapy.

Clinical studies have demonstrated that SGLT2 inhibition improves heart failure outcomes, reduces renal disease progression, and lowers cardiovascular mortality in diabetic patients. The mechanism extends beyond glycemic control, as SGLT2 inhibitors modulate sodium balance, improve endothelial function, and reduce oxidative stress, contributing to enhanced cardiovascular and renal protection. These findings have positioned SGLT2 inhibitors as essential therapies for both diabetic and non-diabetic patients at risk of heart and kidney disease, reinforcing their role as a cornerstone in cardiorenal metabolic management.

Our research is centered on the design and synthesis of small-molecule compounds with potential SGLT2 inhibition. Using AI-driven molecular docking and in-silico screening, we have successfully identified potential hit molecules with good SGLT2 binding affinity. With in-silico evaluation completed and promising molecular characteristics confirmed, our SGLT2 inhibitor is now ready for preclinical investigations, marking a significant step toward a highly effective, therapy for diabetes and its associated cardiorenal complications.

Cardiometabolic disorders, including heart failure, hypertension, and metabolic syndrome, are major global health concerns driven by dysregulated neuro-hormonal signaling and impaired natriuretic peptide activity. One of the key regulators of natriuretic peptide degradation is neprilysin (NEP), a zinc-dependent metalloprotease that breaks down vasodilatory and cardioprotective peptides, such as atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). Excessive neprilysin activity contributes to increased vascular resistance, sodium retention, and cardiac dysfunction, exacerbating the progression of cardiometabolic diseases. Inhibiting neprilysin enhances natriuretic peptide signaling, leading to vasodilation, natriuresis, and improved cardiac function, making it a promising therapeutic strategy for cardiometabolic disorders.

Neprilysin inhibitors have gained significant attention as key modulators of the renin-angiotensin-aldosterone system (RAAS) and natriuretic peptide pathways. The success of combination of NEP inhibitor with angiotensin II receptor blocker (ARNI therapy), has demonstrated superior cardiovascular benefits, including reduced heart failure hospitalizations, improved cardiac output, and lower blood pressure. However, the development of selective small-molecule neprilysin inhibitors remains an active area of research. Next-generation neprilysin inhibitors aim to achieve optimal natriuretic peptide preservation, improve metabolic homeostasis, and provide broader benefits in cardiometabolic disease management.

Our team is dedicated to the iterative development of potent and selective small-molecule neprilysin inhibitor with enhanced selectivity, metabolic stability, and optimized pharmacokinetics. Using AI-driven molecular docking and in-silico screening, we have identified a potential neprilysin inhibitor with high binding affinity. Our Neprilysin inhibitor, refined through in-silico and molecular profiling, is now set for preclinical investigations, representing a significant advancement towards a novel therapy for heart failure, hypertension, and metabolic syndrome.

Obesity is a major global health concern, driving metabolic disorders and significantly increasing the risk of cardiovascular complications, including hypertension, atherosclerosis, and heart failure. One of the most promising therapeutic targets for managing obesity and its associated cardiac risks is the glucagon-like peptide-1 (GLP-1) receptor, a key regulator of glucose metabolism, insulin secretion, and appetite suppression. Activation of GLP-1 signaling enhances insulin sensitivity, reduces food intake, promotes weight loss, and exerts cardioprotective effects by improving endothelial function and reducing inflammation. Given its dual role in metabolic and cardiovascular health, targeting GLP-1 receptors offer a powerful therapeutic strategy for treating obesity while mitigating its cardiac complications.

Approved GLP-1 receptor agonists (GLP-1RAs) have shown remarkable efficacy in weight management and cardiovascular protection. These peptide-based drugs mimic endogenous GLP-1, stimulating insulin secretion, delaying gastric emptying, and promoting satiety. However, despite their success, peptide-based GLP-1RAs have limitations, including poor oral bioavailability, short half-life, and high production costs. This has spurred the development of small-molecule GLP-1 receptor agonists, which offer the potential for oral administration, improved pharmacokinetics, and better patient compliance, expanding the therapeutic reach of GLP-1 targeting beyond injectable formulations.

We are actively engaged in the creation of small-molecule targeting GLP-1 receptor that can mimic the beneficial effects of peptide-based therapies while offering enhanced drug-like properties. Using AI-driven drug discovery and in-silico screening, we have identified potential small molecule GLP-1R agonists with high receptor affinity. Predicted optimum metabolic stability, and favorable oral bioavailability positioning it as a promising candidates for pre-clinical development. By integrating computational modeling, medicinal chemistry, and functional validation, we aim to advance a next-generation GLP-1 therapy that can effectively combat obesity, reduce cardiovascular risk, and provide a convenient, orally available treatment option for patients worldwide.

Alzheimer’s disease (AD) is a devastating neurodegenerative disorder marked by progressive cognitive decline, neuroinflammation, and synaptic dysfunction. Among emerging therapeutic targets, the cannabinoid receptor type 2 (CB2) has gained significant attention for its role in modulating neuroinflammation and protecting against neuronal damage. Unlike CB1, which is primarily found in the central nervous system, CB2 is predominantly expressed in microglia and immune cells, where it regulates inflammatory responses and oxidative stress. Activation of CB2 receptors has been shown to suppress pro-inflammatory cytokines, enhance microglial clearance of amyloid-beta (Aβ), and promote neuroprotection, making it a promising target for AD therapy.

CB2 receptor agonists have demonstrated anti-inflammatory and neuroprotective effects in preclinical AD models, reducing glial activation, tau hyperphosphorylation, and Aβ pathology. Selective CB2 activation has also been linked to improved synaptic plasticity and enhanced cognitive function, highlighting its therapeutic relevance. Despite these benefits, many existing CB2 agonists suffer from poor brain penetration or off-target effects, limiting their clinical utility. The development of highly selective, brain-permeable CB2 agonists represents a significant advancement in targeting neuroinflammation and neuronal survival in AD, with the potential to slow disease progression and enhance neuroprotection.

Our research is focused on developing an AI-designed small-molecule CB2 agonist with enhanced selectivity, optimized pharmacokinetics, and superior blood-brain barrier penetration. Through in-silico screening and molecular docking, we have successfully identified a potential CB2 agonists that exhibits good receptor binding. Our CB2 agonist, optimized through in-silico analysis and molecular refinement, is prepared for preclinical investigations, representing a critical advancement in our pursuit of a novel neuroprotective strategy for Alzheimer's disease.

Chronic stress and stress-related disorders, such as anxiety, depression, and cognitive dysfunction, are closely linked to dysregulated glutamatergic signaling, particularly within the N-methyl-D-aspartate (NMDA) receptor system. Among its subunits, GluN2A, a key component of the NMDA receptor, plays a critical role in synaptic plasticity, excitatory neurotransmission, and stress-induced neuronal excitotoxicity. Excessive GluN2A activation has been associated with heightened neural excitability, increased stress susceptibility, and cognitive impairments, making it a compelling therapeutic target for stress reduction. Selective inhibition of GluN2A offers a novel approach to restoring excitatory-inhibitory balance, alleviating stress-induced neuronal dysfunction, and enhancing emotional resilience.

Targeting GluN2A with small-molecule inhibitors has shown promise in reducing stress-induced overactivation of the NMDA receptor, normalizing glutamate homeostasis, and protecting against stress-related neurotoxicity. Preclinical studies indicate that GluN2A inhibition can modulate synaptic plasticity, reduce hyperexcitability, and improve stress resilience without impairing normal cognitive function. Unlike broad NMDA receptor antagonists, which can cause significant side effects, selective GluN2A inhibitors allow for targeted modulation of stress-related pathways while preserving normal neuronal function. Developing highly selective, brain-penetrant GluN2A inhibitors represents a significant step forward in stress management and mental health therapeutics.

Our research employs advanced AI algorithms to identify and optimize promising small-molecule GluN2A inhibitor, designed to effectively regulate stress-induced glutamatergic dysregulation. Using AI-driven molecular screening and structure-based drug design, we have identified a high-affinity GluN2A inhibitor and favorable ADME properties. With in-silico evaluation successfully completed and molecular optimization achieved, our GluN2A inhibitor is now primed for preclinical investigations, marking an important advancement toward targeted stress-reducing therapies.

Anxiety and stress-related disorders are primarily driven by imbalances in inhibitory and excitatory neurotransmission, leading to hyperactivity in neural circuits regulating fear, stress, and emotional processing. One of the most crucial regulators of neuronal inhibition is the gamma-aminobutyric acid type A (GABAA) receptor, a ligand-gated chloride channel that mediates fast inhibitory neurotransmission in the brain. Dysfunction or reduced activity of GABAA receptors has been linked to heightened anxiety, excessive neural excitability, and impaired stress resilience, making GABAA receptor activation a highly effective strategy for restoring calmness and emotional stability. By enhancing GABAergic signaling, selective GABAA receptor agonists can rebalance neural circuits, reduce anxiety symptoms, and promote relaxation.

GABAA receptor agonists, including benzodiazepines, barbiturates, and neurosteroids, have long been used to treat anxiety, insomnia, and panic disorders due to their ability to enhance GABAergic inhibition and suppress excessive neuronal firing. However, traditional GABAA receptor agonists pose challenges such as sedation, dependence, and cognitive impairment, necessitating the development of next-generation GABAA agonists with improved safety and efficacy profiles. Selective GABAA receptor subtype agonists targeting α2 and α3 subunits have shown anxiolytic effects without the sedative or addictive risks associated with non-selective modulators, representing a breakthrough in next-generation anxiety therapeutics.

We are streamlining small-molecule drug discovery through AI-enabled virtual screening and optimization of novel small-molecule GABAA receptor agonist. It designed to enhance inhibitory neurotransmission while minimizing sedation and dependence risks. Using AI-driven molecular screening and computational drug design, we have identified a high-affinity GABAA agonist with optimized receptor selectivity and favorable pharmacokinetic properties. Our GABAA receptor agonist, having successfully completed in-silico evaluation and molecular refinement, is now poised for preclinical studies, marking a significant step forward in developing novel anxiety and stress therapies

Epilepsy is a chronic neurological disorder characterized by abnormal, excessive neuronal excitability, leading to recurrent seizures and impaired neural function. One of the key regulators of inhibitory neurotransmission in the brain is the GABA transporter-1 (GAT1), which is responsible for GABA reuptake from the synaptic cleft into presynaptic neurons and glial cells. Overactive GAT1 function leads to excessive GABA clearance, reducing inhibitory signaling and increasing the risk of seizure generation. Targeting GAT1 inhibition offers a promising therapeutic strategy for restoring GABAergic tone, preventing hyperexcitability, and reducing seizure frequency in epilepsy patients.

Selective GAT1 inhibitors have demonstrated significant potential in enhancing extracellular GABA levels, thereby prolonging inhibitory neurotransmission and stabilizing neural activity. Existing GAT1 inhibitors have challenges such as limited brain penetration, off-target effects, and dose-dependent side effects highlight the need for next-generation small-molecule GAT1 inhibitors with improved efficacy and safety profiles. Developing highly selective, brain-permeable GAT1 inhibitors represents a major advancement in precision epilepsy treatment, providing long-term seizure control with minimal side effects.

We are in the initial phase of developing a novel small-molecule GAT1 inhibitor designed to enhance GABAergic neurotransmission and prevent seizure initiation. Using AI-driven molecular design and in-silico screening, we have successfully identified a high-affinity GAT1 inhibitors with favorable ADME properties. With in-silico evaluation successfully completed and molecular refinement achieved, our GAT1 inhibitor is now ready for preclinical investigation, marking an important step toward a safer, more effective treatment for epilepsy and seizure disorders.

Migraine is a debilitating neurological disorder characterized by intense headaches, sensory sensitivity, and nausea, often triggered by abnormal activation of pain pathways and neurovascular dysregulation. One of the key molecular drivers of migraine is the calcitonin gene-related peptide receptor (CGRPR), which plays a crucial role in vasodilation, neurogenic inflammation, and pain transmission. Elevated CGRP levels during migraine attacks contribute to prolonged blood vessel dilation and hypersensitivity in the trigeminal pain pathway, making CGRPR a prime therapeutic target. Blocking CGRPR signaling has been shown to effectively prevent and relieve migraine symptoms, offering a targeted approach for long-term migraine management.

The development of CGRPR antagonists has transformed migraine therapy, with monoclonal antibodies and small-molecule CGRPR antagonists demonstrating significant clinical efficacy in acute and preventive migraine treatment. Unlike traditional treatments, CGRPR antagonists do not cause vasoconstriction, making them safer for patients with cardiovascular risk factors. However, there remains a need for next-generation CGRPR antagonists with enhanced selectivity, improved brain penetration, and optimized pharmacokinetics to further enhance efficacy and minimize side effects. Developing highly potent and long-lasting CGRPR inhibitors represents a major advancement in migraine treatment.

We are currently developing a novel small-molecule CGRPR antagonist designed to selectively block CGRPR signaling, reduce neurogenic inflammation, and prevent migraine attacks. Using AI-driven molecular docking and in-silico screening, we have successfully identified a high-affinity CGRPR antagonist with optimized receptor binding and favourable pharmacokinetic properties. Our CGRPR antagonist has advanced through computational evaluation and molecular refinement, and is now prepared for preclinical investigation, representing a major milestone in our quest for innovative migraine treatments.