Fabre-Kramer Pipeline

Diversified Portfolio of compounds addressing unmet needs in various stages.



FKB01MD: Phase 2


EXXUA™: Phase 3

FKW00GA: Phase 2


EXXUA™ (HSDD): Phase 2

FKF02SC: Phase 1

FKK01PD: Pre-Ind

In Phase II & III, 3100 patients have been treated with EXXUA™ formerly known as Travivo. In addition, 634 children and adolescents were enrolled into pediatric trials in depression. The extensive clinical experience with EXXUA™ has shown it free of troublesome adverse events.

EXXUA™ for Major Depression
EXXUA™ for Generalized Anxiety Disorder
EXXUA™ for Hypoactive Sexual Desire Disorder

Therapeutic Area: Major Depression

  • Development Status: Phase II, Extended Release prototypes are in development.

Production Description

Over the past 25 years, progress in the treatment of major depression has been limited to an improvement in the side effect profile. The serotonin reuptake inhibitors, while safer than imipramine and other tricyclics, are less efficacious.

Forty percent or more of major depression patients do not respond to currently available antidepressants. There is a need for an antidepressant with stronger activity that could treat a larger selection of depressed patients.

FKB01MD is a strong antidepressant that down regulates 5HT2 receptors in animals overnight. FKB01MD has 5 mechanisms of action including 5HT reuptake blockade, 5HT2 agonism, 5HT1A agonism, and actions on the 5HT1D central receptors. FKB01MD is active in the usual animal models of depression especially in the ability to inhibit muricidal behavior (i.e. mouse killing) in rats where it is more active than fluoxetine or desipramine. It was also more active than SSRIs in the Porsolt test.

The robust efficacy demonstrated by FKB01MD in animal models that predict antidepressant potential in man is believed to reflect this drug’s multiple interactions with serotonergic mechanisms. This multiplicity of action consists of the incorporation of several distinct serotonergic mechanisms found in other clinically effective antidepressants into a single molecule, FKB01MD. This agent exhibits the 5HT reuptake blockade found in tricyclic antidepressants, 5HT2 receptor blockade found in trazodone, and 5HT1A interactions found in azapirones. Additionally, FKB01MD exhibits a unique agonist interaction with the central terminal 5HT1D autoreceptor. It is anticipated that the interactions of FKB01MD with multiple subtypes of 5HT2 receptors will produce earlier and greater adaptation of serotonergic systems than other antidepressants, and this will in turn result in a more rapid onset and greater degree of antidepressant efficacy.

Clinical Trials

Phase I studies indicate no areas of concern. Pharmacokinetic studies indicate the absolute bioavailability is approximately 17% and the half-life is approximately 4 hours. Adverse events were mild and mostly limited to lightheadedness and nausea. Several short term Phase II efficacy studies have been performed. Doses of 10-30 mg BID were well tolerated by depressed patients. In certain patients in the Phase II studies the drug showed strong antidepressant activity.


Developmental and licensing opportunities are available.

Therapeutic Areas: Anxiety, Social Phobia, Sexual Dysfunction

  • Development Status: Phase II

Product Description

FKW00GA is unique in that it will be the first 5HT1A Agonist and 5HT2 Antagonist on the market for the treatment of anxiety. FKW00GA’s mechanism of action indicates that this product would be beneficial for both anxiety and sexual dysfunction. Initially, this product will be developed for social phobia. After the product is on the market, FKP plans to register it for other indications such as generalized anxiety disorder, mixed anxiety depression and sexual dysfunction.

FKW00GA is a nonbenzodiazepine anxiolytic that should not have benzodiazepine-like or anticholinergic side effects. Preclinical studies have shown it to have a very high affinity for the serotonin 1A (5HT1A) receptor. In addition, FKW00GA has a high affinity for the serotonin 2 (5HT2) receptor. The 5HT1A partial agonist and 5HT2 antagonist activities of FKW00GA suggest the agent will have beneficial properties for the treatment of anxiety and sexual dysfunction.

Clinical Trials

In Phase I trials, FKW00GA is safe and tolerated up to single doses of 180 mg and multiple doses of 60 mg T.I.D. for 7 days. Adverse effects were minimal consisting mostly of light headedness and nausea. Several Phase II studies were conducted in generalized anxiety disorder. Signals indicating efficacy were found. Phase III protocol for the existing formulation has been submitted to FDA. An extended release formulation will achieve better patient compliance and a lower side effect profile. Presently, several different extended release prototypes are in development. A new formulation will help to maximize the market potential of this drug.


Developmental and licensing opportunities are available.

Therapeutic Area: Schizophrenia

  •  Development Status: Phase II

Product Description

FKF02SC is a 5HT2/D2 atypical antipsychotic. Like other atypical antipsychotics, FKF02SC has the highest receptor binding for the dopamine D2 and D3 receptors, the serotonin 5HT2C and 5HT2A receptors, the adrenergic 1 receptor and the histamine H1 receptor, and is moderate affinity for the D1, D4 and 5HT1A receptors as well.

FKF02SC exhibited dose-related antipsychotic activity in several animal behavioral models. FKF02SC inhibited amphetamine-induced hyperactivity in mice over a dose range of 0.0625 to 0.5 mg/kg (ID50 value = 0.16 mg/kg). Its activity was similar to that of risperidone and haloperidol, and greater than that of clozapine. The ability of FKF02SC (0.0625 to 0.5 mg/kg) to inhibit apomorphine-induced climbing behavior in mice and apomorphineinduced hyperactivity in mice suggested its potential beneficial effects on the positive symptoms of schizophrenia. Because of its alpha-adrenergic antagonist activity, FKF02SC protected mice against noradrenaline-induced lethality (ED50=0.05 mg/kg); this implied a potential to mitigate the positive symptoms and ameliorate the cognitive symptoms of schizophrenia; its potency in this test was similar to that of risperidone. FKF02SC also inhibited MK-801-induced hyperactivity in mice (ID50=0.23 mg/kg), which indicated its potential beneficial effect on the negative symptoms of schizophrenia. FKF02SC inhibited the 5HT2A receptor in the DOI-induced head twitch test in mice. This suggested that FKF02SC might provide an amelioration of both positive and negative symptoms of schizophrenia with a low incidence of extrapyramidal symptoms. FKF02SC also demonstrated 5HT2C receptor antagonism in the mCPP-induced hypolocomotion test in rats.

FKF02SC did not protect mice against physostigmine-induced lethality at oral dosages of 4 or 8 mg/kg. This 8 mg dose was approximately 33 times the ID50 value for FKF02SC with respect to the inhibition of apomorphine-induced climbing behavior (0.24 mg/kg), which is associated with antipsychotic activity. This implied that FKF02SC would have a low incidence of antimuscarinic side effects at effective antipsychotic doses. The ID50 value for FKF02SC (18.40 mg/kg) with respect to apomorphine induced climbing assay in mice, indicates a potential lack of extrapyramidal side effects at antipsychotic doses. FKF02SC showed an antagonistic effect on dopamine D1 receptors (ID50 = 0.31 mg/kg) in the SKF38393-induced grooming test in mice, which suggested a possibility of lesser extrapyramidal side effects.

Clinical Trials

Three Phase I trials have been conducted in normal healthy males. Two were single dose, dose escalation studies and the third was a multiple dose, dose escalation study. The single dose studies showed that in the oral dose range 0.5 to 1.5 mg pharmacokinetics were linear with Tmax between 2 and 4 hours and 1/2 between 2 and 3 hours. In the multiple dose study, 0.5, 1.0, or 1.5mg was given daily for 7 days. FKF02SC was rapidly absorbed with Tmax of about 2.5 hours and 1/2 from 3.24 to 3.84 on both days 1 and 7. There was no accumulation. In both studies, the most frequent adverse event was postural hypotension manifested by increased heart rate, decreased standing blood pressure, and in some cases dizziness. Electrocardiographic examinations revealed no abnormalities, including no changes in QTc.


Developmental and licensing opportunities are available.

Therapeutic Areas: Parkinson’s disease and Erectile Dysfunction

  • Development Status: IND in preparation

Product Description

FKP has a goal to develop an apomorphine pro drug with prolonged therapeutic antiparkinson effects suitable for delivery orally (once a day),transdermally (once a week) and as an implant (once every six months). Also, the drug should produce near complete relief of Parkinson symptoms without dyskinesias. To this end, FKP has the patent rights to a large series of apomorphine monoesters and mixed esters.
The lead compound, FKK01PD, is an orally active postsynaptic D1 and D2 agonist. The drug has a similar action to apomorphine without the toxicity and short duration of activity of apomorphine.
In freely moving rats with an indwelling interstitial cannula, FKK01PD, given orally in enteric coated capsules showed obvious behavioral signs of dopamine stimulation for at least 10 hours. Dopamine and DOPAC measured by HPLC from the cannula showed significant decreases indicating dopamine receptor agonism.
Three studies have been conducted on MPTP lesioned levodopa treated marmoset’s at Dr. Tom Chase’s lab at the NIH. FKK01PD given orally in an enteric coated capsule produced optimal antiparkinson activity for 33 hours. Multiple dosing for 7 days produced excellent results with a 28 hour “on” after the last dose. A pharmacokinetic study in these animals demonstrated blood levels out to 36 hours. These results indicate that this is an important compound which could be moved along quickly. The manufacturing, pharmacology and toxicology are
ready for IND preparation.

Clinical Trials

Protocols in development.


Developmental and licensing opportunities are available.