OUR PIPELINE



acu-D2
Systemic Scleroderma



We have discovered and validated that a deficit in the mitochondrial deacetylase Sirtuin 3 (SIRT3) is a pathogenic mechanism underlying fibrosis in Systemic Scleroderma in humans and that SIRT3 has cell-intrinsic potent anti-fibrotic properties.

  • Our novel compound ACU-D2 stimulates SIRT3 expression in a dose dependent manner
  • displays inhibitory TGF-ß-induced fibrotic responses/signaling in fibroblasts, and effects on mitochondrial ROS generation.
  • Attenuates fibrosis and restores SIRT3 levels in preclinical mouse models and been has
  • Validated via knock out models.
  • ACU-D2 potentially offers a novel new therapeutic option for the treatment of Systemic Scleroderma.


ACU D2 Neurodegenerative Diseases





Mechanism of action



Alzheimer's Disease

ACU D2 has the potential to transform the treatment of AD resulting in a higher cognitive function, better quality of life, and reduction of the finical burden to society for the treatment of this devastating disease.

  • Mitochondrial dysfunction has been closely linked to the pathogenesis of AD, and recent studies have shed new light on the relationship between SIRT3 and mitochondrial function and neuronal activity in AD. Results indicate that SIRT3 dysfunction leads to mitochondrial and neuronal damage in AD.
  • Sirt3 mRNA and protein expression in multiple Brain regions were significantly lower in AD compared to those in cognitively normal subjects. We also identified a strong association between Sirt3 and cognition along with a clear inverse correlation between Sirt3 and tau pathology. These results that Sirt3 may be a novel player in the pathogenesis of AD.

Preclinical Studies have demonstrated that ACU D2:

  • Inhibits the activity of GSK-3β, a key signaling event implicated in tau hyperphosphorylation.
  • Reduces the Amyloid beta levels (BACE 1 activity & Abeta42) in a dose dependent manner.
  • SIRT3 participates in an endogenous neuroprotective response, SIRT3 expression can attenuate AD-related pathological events.
  • ACU-D2 has validated efficacy in multiple in vivo models of AD by activating SIRT3 signaling in the hippocampus and cerebral cortex.

Parkinson's Disease

ACU-D2 Demonstrated Efficacy in Parkinsonian Rat model have validated the protective role in PD where ACU-D2

  • Prevented loss of motor coordination and
  • Prevents loss of sensory motor function.


HIV-Associated Neurocognitive Disorder

ACU-D2 Demonstrated Efficacy In HIV induced mouse model as a potential first in class therapeutic for the treatment of HIV-Neurocognitive Disorder

  • Mice were tested to assess cognitive function by seeing if they could recognize a novel object in a familiar environment Cognitive abnormalities seen in HAND mice were significantly reversed by ACU-D2
  • ACU-D2 demonstrated efficacy in key HAND Biomarkers Significantly reduced the astrogliosis, ameliorated the neuronal abnormalities, and inhibited the activation of monocular phagocytes
  • Systemic Administration Feasible: Readily permeate the blood brain barrier and the blood-cerebrospinal fluid
  • Novel new nano-emulsion targeting intranasal and systemic administration.

We are currently performing additional pre-clinical research and IND enabling development activities.



ACU-D3
melanoma: Vemurafenib Resistant



Our compound inhibits the phosphorylation of DRP1, thus stimulating a phenotype suggestive of respiration through mitochondrial normalization. Acts selectively in vemurafenib resistant melanomas to increase both respiration and prevents from becoming glycolitic, leading to activity against aggressive resistant melanoma in vivo.

  • The most prevalent melanoma mutation is BRAF (V600E) which constitutively activates downstream MAPK signaling,
  • New targeted therapies have been developed to inhibit BRAF signaling and downstream pathways. These drugs often produce dramatic responses, but unfortunately, these responses usually last for a few months.
  • Our compounds: demonstrated significant antitumor activity in vivo against A375 malignant melanoma.
  • ACU-D3 demonstrates significant antitumor activity in vivo against vemurafenib-resistant melanoma LM36R. Suggesting acquired signaling differences through resistance of BRAF inhibition.

We are currently performing additional pre-clinical research and IND enabling development activities.



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